Hemp has been called a plant of “major economic importance,” as it grows like a weed, yet can be used in the production of food, personal care products, textiles, paper, and even plastic and construction materials.1
Valued since ancient times as a fiber source for textiles, the hemp industry eventually made it to the US, where it flourished in the mid-1800s, through World War I and again briefly during World War II, when the war cut off supplies of fiber.2
In the US, the cultivation of hemp has been banned since the 1970s when the federal Controlled Substances Act took effect. The law doesn’t distinguish between marijuana, the drug, and hemp, the plant, despite major scientific differences.
Ironically, the US is the world’s largest consumer of hemp products, yet is the only industrialized country that also outlaws its production. As a result, all US hemp products – a more than $600-million market in the US – are imported.3 As noted in “Hemp: A New Crop with New Uses for North America:”4
“Cannabis sativa [hemp] is extremely unusual in the diversity of products for which it is or can be cultivated. Popular Mechanics magazine (1938) touted hemp as ‘the new billion dollar crop,’ stating that it ‘can be used to produce more than 25,000 products, ranging from dynamite to Cellophane.'”
What’s the Difference Between Hemp and Marijuana
Hemp and marijuana come from the same plant species, Cannabis sativa, but there are noted differences between the two plants. They both contain cannabidiol (CBD), which has medicinal properties. The amount of CBD however, differs greatly between the two.
Dosing, therefore, is dramatically different when you to try to use hemp in lieu of cannabis for medicinal purposes, as the latter, cannabis, is up to 100-fold more potent.
Another difference that appears to matter in terms of its usefulness as medicine relates to differing terpene profiles. Hemp contains very little of these valuable medicinal compounds.
Lastly, there’s the tetrahydrocannabinol (THC) content. THC is the psychoactive component of marijuana; it’s the molecule that makes you feel “stoned.” (While cannabidiol (CBD) also has certain psychoactive properties.
It does NOT produce a high.) By legal definition, hemp cannot have more than 0.3 percent tetrahydrocannabinol (THC) in it. So to summarize:
- Hemp has less value for medicinal uses, as it only contains about 4 percent CBD and lacks many of the medicinal terpenes and flavonoids.It also contains less than 0.3 percent THC, which means it cannot produce a high or get you stoned. While hemp may not have the same medicinal uses as marijuana, it does have excellent nutritional value that may boost health.
- Marijuana can act as a potent medicine courtesy of high amounts (about 10 to 20 percent) of CBD, critical levels of medicinal terpenes, and flavonoids, as well as THC in varying ratios for various diseases. The higher the THC, the more pronounced its psychoactive effects.
- Genetic Difference Between Hemp and Marijuana Uncovered
If there were still any question over whether or not hemp and marijuana are two different plants, it should be put to rest with the publication of a new study that shows the genetic difference between hemp and marijuana.5
Researchers from the University of Minnesota’s (U of M) College of Biological Sciences and College of Food, Agricultural, and Natural Resource Sciences belong to one of the few groups of US scientists that have been granted federal clearance to study cannabis.
After more than 12 years of research, the team found a single gene that is responsible for the genetic differences between hemp and marijuana. As noted by Medical Daily:6
“While hemp produces a non-euphoric cannabidiol (CBD) with approximately 0.3 to 1.5 percent tetrahydrocannabinol (THC) concentration, marijuana is packed with between five to 10 percent (or even higher) psychoactive THC concentration.”
The researchers believe they have “indisputable evidence” that hemp and marijuana should be regarded as separate plants.
Nearly half of US states now separate hemp from marijuana. George Weiblen, a professor with a joint appointment in the U of M’s College of Biological Sciences and College of Food, Agricultural and Natural Resource Sciences, said:7
“It’s a plant of major economic importance that is very poorly understood scientifically… With this study, we have indisputable evidence for a genetic basis of differences among cannabis varieties, further challenging the position that all cannabis should be regulated as a drug.”
- Health Benefits of Hemp
One of the under-appreciated benefits of hemp, at least in the US, is as a food source. Hemp seeds, which are technically a nut and are also known as “hemp hearts,” are rich in healthy fats, protein, and minerals.
Hemp seeds are usually consumed after the hard outer shell is removed, leaving just the soft, creamy “heart” behind. The seeds have a slight nutty flavor, making them incredibly versatile for use in cooking, baking, or for adding to smoothies and salads. Some of their primary health benefits include:8
- Excellent Source of Nutrition
Hemp seeds are composed of more than 30 percent healthy fats, including the essential fatty acids linoleic acid and alpha-linolenic acid (plant-based omega-3). According to research published in Nutrition & Metabalism
“Dietary hempseed is… particularly rich in the omega-6 fatty acid linoleic acid (LA) and also contains elevated concentrations of the omega-3 fatty acid α-linolenic acid (ALA). The LA:ALA ratio normally exists in hempseed at between 2:1 and 3:1 levels. This proportion has been proposed to be ideal for a healthy diet.”
Hemp seeds also contain gamma-linolenic acid, which supports the normal function and growth of cells, nerves, muscles, and organs throughout your body.
Hemps seeds are about 25 percent protein and also provide nutrients including vitamin E, phosphorus, potassium, magnesium, sulfur, calcium, iron, and zinc.
- Heart Health
- Hemp seeds contain numerous heart-healthy compounds, including the amino acid arginine. L-arginine is a precursor to nitric oxidein your body. It has been shown to enhance blood flow and help you maintain optimal blood pressure. Nitric oxide signals the smooth muscle cells in your blood vessels to relax, so that your vessels dilate and your blood flows more freely.
- This helps your arteries stay free of plaque. When you have inadequate nitric oxide, your risk for coronary artery disease increases. The gamma-linolenic acid found in hemp seeds is anti-inflammatory, another bonus for heart health. Past research has also shown hemp seeds may help reduce blood pressure, decrease the risk of blood clots, and boost recovery after a heart attack.
- Skin Health
- Fatty-acid deficiency can manifest in a variety of ways, but skin problems such as eczema, thick patches of skin, and cracked heels are common. Hemp seeds are a rich source of fatty acids in the optimal omega-6 to omega-3 ratio. Research suggests hempseed oil may improve symptoms of atopic dermatitis10 and potentially provide relief from eczema.
- Plant-Based Protein
- Although I believe protein from high-quality animal sources is beneficial for most people, if you are following a plant-based diet, hemp makes a healthy source of protein. With all of the essential amino acids and an amount of protein similar to beef (by weight), hemp seeds are an excellent form of plant-based protein.
- Two to three tablespoons of hemp seeds provides about 11 grams of protein, complete with the amino acids lysine, methionine, and cysteine. Two main proteins in hemp seed protein, albumin and edestin, are rich in essential amino acids, with profiles comparable to soy and egg white. Hemp’s edestin content is among the highest of all plants. Hemp protein is also easy to digest because of its lack of oligosaccharides and trypsin inhibitors, which can affect protein absorption.
- PMS and Menopause Symptoms
- The gamma-linolenic acid (GLA) in hemp seeds produces prostaglandin E1, which reduces the effects of the hormone prolactin. Prolactin is thought to play a role in the physical and emotional symptoms of premenstrual syndrome (PMS). GLA in hemp seeds may also help reduce the symptoms of menopause. 11
- Whole hemp seeds contain both soluble and insoluble fiber, which may support digestive health and more. Soluble fiber dissolves into a gel-like texture, helping to slow down your digestion. This helps you to feel full longer and is one reason why fiber may help with weight control. Insoluble fiber does not dissolve at all and helps add bulk to your stool. This helps food to move through your digestive tract more quickly for healthy elimination.
- Fiber plays an essential role in your digestive, heart, and skin health, and may improve blood sugar control, weight management, and more. Please note that only whole hemp seeds contain high amounts of fiber; the de-shelled hemp seeds or “hearts” contain very little fiber.
Agricultural Hemp Returns to Kentucky
Kentucky was once home to a flourishing hemp industry, but once hemp was outlawed, tobacco became the go-to cash crop. That is now slowly changing once again, as farmers take advantage of the five-year pilot Industrial Hemp Research Program, which was established by James Comer, Kentucky’s commissioner of Agriculture.12 The program is one recently launched in a number of states, where permission has been granted for industrial hemp to be grown for research purposes. As reported by Newsweek:13
“Kentucky led the U.S. industrial hemp business until the end of the Civil War, when production of the crop declined and was generally replaced by tobacco. The Marihuana Tax Act of 1937 put the kibosh on all production and sales of cannabis, including industrial hemp, but the crop saw a rapid resurgence during World War II. Hemp fiber became essential to produce military necessities such as uniforms and parachutes.
The U.S. Department of Agriculture launched its national ‘Hemp for Victory’ program, which provided seeds and draft deferments to farmers. In 1942, farmers planted 36,000 acres of hemp seed. A USDA-funded informational film from that year noted that ‘hemp grows so luxuriantly in Kentucky that harvesting is sometimes difficult.'”
Comer reportedly wants to “single-handedly turn industrial hemp into Kentucky’s No. 1 cash crop” and “breathe new life into family farms that have lost millions of dollars with the fall of the tobacco industry.”14
Currently, most industrial hemp comes from China, but the plant could bring great economic growth to areas of the US. Among the many products provided by industrial hemp are:
- Cannabidiol (CBD), the medicinal compound, which can be extracted from the leaves, blossoms, and stems
- Cannabis oil, which comes from cold-pressing the seeds and can be used for cooking, cosmetics, and beauty products
- Fiber, which can be used as a substitute for cotton, wood, and plastic, with potentially endless uses
- Hemp seeds, which are poised to become a human superfood and could also be used in animal feed
Hemp Could Provide an Environmentally Friendly Alternative to Plastic Hemp plastic is a “material of the future” that could drastically cut down on the need for plastics and their devastating toll on the environment. In some cases, standard plastics may be reinforced with hemp, which may account for up to 80 percent of the plastic’s weight. Hemp can also be used to make 100 percent hemp plastic, which is recyclable and can be 100 percent biodegradable.
Currently, the most common type of hemp plastics are those infused with hemp fibers, which means less plastic is used and the resulting product is more durable (hemp plastic is said to be five times stiffer and 2.5 times stronger than polypropylene).15 According to Hempowered.com:16
“Using sustainable and renewable natural plant fibers (such as hemp, flax, jute, and kenaf) and through industrial production techniques that mix them into plastics, a new award winning (Biomaterial of the year 2010) granule has been made from a combination of hemp with polypropylene, thus reducing the use of petroleum products.
… Their recoverable component comes from these natural plants and can make up over half of their weight, up to 80 percent. All these features make them suitable for the production of durable products. Hemp Plastic granules offer many advantages like good insulation, dimensional stability at high temperatures, a high thermal deformation temperature, and impermeability… The granules are currently produced for a range of applications in automobiles, construction materials, packaging, toys, and electronic products and launched onto the market in 2010.”
Hemp Could Soon Be Reclassified As an Agricultural Crop
Currently, hemp can only be grown in select US states for research purposes. However, even then the US Drug Enforcement Administration makes it challenging for growers. According to Newsweek:17
“The DEA’s cannabis eradication program provides funding to local law enforcement to form a SWAT team of ‘cowboys flying around in helicopters.’ They have been known to sweep through private farms to confiscate the plants, and have even been known to mistake okra for marijuana.”
A bill in Congress could change that as, if passed, it would reclassify hemp from a narcotic to an agricultural crop. Rep. Jared Polis (D-Colo.), a co-sponsor of the bill – the Industrial Hemp Farming Act of 2015 — told the Huffington Post:18
“The federal ban on hemp has been a waste of taxpayer dollars that ignores science, suppresses innovation, and subverts the will of states that have chosen to incorporate this versatile crop into their economies… I am hopeful that Congress will build on last year’s progress on hemp research and pilot programs by passing the Industrial Hemp Farming Act to allow this historical American crop to once again thrive on our farmlands.”
- 1, 3, 6, 7 Medical Daily July 20, 2015
- 2, 4 Trends in new crops and new uses, 2002, Hemp: A new crops with new uses for North America
- 5 New Phytologist July 17, 2015
- 8 Authority Nutrition September 2015
- 9 Nutr Metab (Lond). 2010; 7: 32
- 10 J Dermatolog Treat. 2005 Apr;16(2):87-94
- 11 Methods Find Exp Clin Pharmacol. 2010 Sep;32(7):467-73
- 12, 13, 14, 17 Newsweek October 11, 2015
- 15, 16 Hemppowered.com Hemp Plastic Solution
- 18 Huffington Post January 22, 2015
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A team of US and Brazilian researchers have used a synthetic sex hormone to stimulate production of a naturally occurring enzyme called telomerase that is capable of reversing ageing and has been dubbed a possible “cellular elixir of youth.”
While in embryos, telomerase is expressed by practically every cell. It can then only be produced in cells that are constantly dividing, such as blood-forming stem cells, which can differentiate into various specialized cells, scientists say. Certain cells avoid aging by using telomerase to lengthen their telomeres, which are DNA-protecting structures at the ends of chromosomes. The length of telomeres is a laboratory measure of a cell’s age, as each time a cell divides, its telomeres get shorter.
“In a healthy adult, telomere length varies from 7,000 to 9,000 base pairs on average. A normal person’s telomeres lose 50 to 60 base pairs per year, but a patient with telomerase deficiency can lose between 100 and 300 base pairs per year,” said Professor Rodrigo Calado, one of the scientists behind the research, the results of which were published in the New England Journal of Medicine.
Telomerase deficiency may cause some blood-related diseases, such as aplastic anemia. In the recent study, scientists treated 27 patients having telomere diseases with a steroid called danazol, a synthetic male hormone, leading to telomere elongation.
“In the patients who received danazol, telomere length increased by 386 base pairs on average over two years,” Calado said.
The research was based on previous findings that showed that androgens, which are converted into estrogens in humans, bind to female hormone receptors in the telomerase gene promoter region, stimulating expression of the enzyme in cells. The latest study “was designed to find out whether the effect we’d observed in the lab also occurred in humans, and the results indicate that it does,” the professor said.
While finding that sex hormones may be used to reverse one of the biological drivers of aging, researchers are cautious, as the risks of using the treatment in healthy people are not yet clear.
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By Dr. Mercola
It is now estimated that 1 in 8 Americans are on serotonin reuptake inhibitors (SSRI) antidepressants1 and a shocking 1 in 4 among women in their 40s and 50s.2 Yet the U.S. suicide rate of 38,000 a year has never been higher.3
Clearly the glut of SSRI prescriptions is not lowering the national suicide rate; rather there is compelling evidence that the popular pills are actually contributing to suicide.
SSRIs and Violence
The first suspicion that SSRIs can cause dangerous and unintended psychiatric effects was a Kentucky shooting in 19894 in which pressman Joseph T. Wesbecker entered his former workplace, Standard Gravure, killed eight people, injured 12 and committed suicide after being prescribed Prozac.
Families of the wounded and killed soon filed a lawsuit against Prozac maker Eli Lilly and Company, claiming the SSRI contributed to the violence. The case went to a jury that sided with Lilly.
Yet three days before the shooting, Wesbecker’s psychiatrist had written “Prozac?” in his patient notes as a possible explanation of his bizarre behavior.
Since the Standard Gravure killings, psychiatrists, drug safety advocates and bereaved families have consistently tried to expose links between SSRIs and suicides but are hampered by mainstream safety data that deny a suicide link.
Study Suggests ‘No Suicide Link’ Is Not to Be Trusted
However, a recent study suggests the “no suicide links” findings are not necessarily to be trusted, noting that: “Therapists should be aware of the lack of proof from RCTs (randomized control trials) that antidepressants prevent suicides and suicide attempts.”5
Dr. David Healy, professor of psychiatry at Bangor University and author of 20 books including “The Antidepressant Era,” “The Creation of Psychopharmacology,” “Let Them Eat Prozac,” “Mania,” and “Pharmageddon,” heartily agrees that the SSRI statistics given to the public is problematic.6
“People haven’t had access to the data. There have been no publications around it. This is one of the biggest problems on which there’s a huge amount of data, but to which we’ve got little or no access …
If we were getting our drug information from The New York Times instead of medical journals, we would all be a lot safer. When the Times reporter Jayson Blair was found to have fabricated stories, he was history.
But the editors and writers involved with journal fraud still have their jobs and the articles are not even retracted. In fact, Liz Wager, Ph.D., the chair of the Committee on Publication Ethics (COPE) is herself Pharma-linked.”
The COPE website said about Wager,7 its former chair, “Liz provides writing, editing, training and consultancy services for various pharmaceutical companies” (most recently AstraZeneca, Cephalon, Cordis Corporation, GlaxoSmithKline, Eli Lilly, Janssen-Cilag, Merck Serono, Mundipharma, Norgine, Novo Nordisk, Sanofi Pasteur and Vifor Pharma) at the time of the interview with Healy.
Healy estimates as many as 1,000 to 2,000 Americans on SSRIs kill themselves each year, when they otherwise would not have done so. Violent acts against others and birth defects are also linked to the pills, he says.
Suicides Linked to Antidepressants Number in the Thousands
Even as high level links between medical editors and the drug industry prevented accurate information from reaching the public, in 1997, drug safety activists launched a website called SSRIstories.com,8 which archived credible and published reports that cite the role of SSRIs and related antidepressants in suicides and other violent behavior.
There are now thousands of entries. “The kind of energy, rage and insanity seen in a lot of crimes today was not seen before SSRIs appeared,” said Rosie Meysenburg, a founder of the website in an interview shortly before her death.9
In addition to the thousands of suicides, “there are two cases of women on the SSRI Stories site who stab a man close to 200 times and a case of a man who stabs his wife over 100 times and then goes next door to the neighbor’s house and stabbed the neighbor’s furniture about 500 times.”
The SSRI stories archive includes people on SSRIs setting themselves on fire, violent elderly people (which is rare) and bizarre cases of kleptomania and female school teachers molesting their minor male students. The common denominator in all the recorded crimes is the drug.
Drug companies routinely blame suicides on the depression that was being treated, not the drugs — but the experiences of patients treated with the same drugs for non-mental indications like pain and the experiences of healthy volunteers cannot be written off as the “disease.”
The Dark Side of Cymbalta
In 2004, 19-year-old Traci Johnson who had no history of mental problems hung herself in the Eli Lilly Clinic in Indianapolis while testing the drug giant’s serotonin–norepinephrine reuptake inhibitor (SNRI) duloxetine, sold under the brand name Cymbalta, a type of antidepressant similar to SSRIs.10
The suicide did not delay the drug’s approval and wide use. In 2008, the Journal of Clinical Psychopharmacology describes a 37-year-old man with a stable marriage, stable employment and no history of mental problems trying to kill himself two months after being prescribed Cymbalta for back pain.
“The patient was unable to state exactly why he wanted to commit suicide,” wrote the four physician authors in the report, also noting that the man returned to normal when the drug was stopped.
The authors also report a 63-year-old man with no mental health history becoming suicidal two weeks after being put on Cymbalta for fatigue, insomnia and sadness, yet he too was “unable to explain why he was having thoughts of wanting to die.”
Other cases of healthy people committing suicide on Cymbalta have been reported11 and many still remember the suicide of Carol Gotbaum at Phoenix’s Sky Harbor International Airport who was on the drug. She was the stepdaughter-in-law of New York City’s public advocate at the time, Betsy Gotbaum.
Writing for Slate, reporter Jeanne Lenzer identified 13 suicides12 linked to Cymbalta besides Traci Johnson. Eli Lilly wanted to market the drug as a treatment for urinary incontinence too but withdrew its application and would not release the study data to Lenzer, she says. It may well have contained more evidence of suicide side effects.
The Drug Industry Still Fights Black Box Warnings Added in 2004
In 2004,13 in response to the outcry over antidepressant-linked suicides, the U.S. Food and Drug Administration (FDA) directed drug makers to add a “Black Box” warning to SRRIs and related psychiatric drugs, highlighting suicide risks and the need for close monitoring of children and adolescents for suicidal thoughts and behavior.
“Today’s actions represent FDA’s conclusions about the increased risk of suicidal thoughts and the necessary actions for physicians prescribing these antidepressant drugs and for the children and adolescents taking them.
Our conclusions are based on the latest and best science. They reflect what we heard from our advisory committee last month, as well as what many members of the public have told us,” said Dr. Lester M. Crawford, acting FDA commissioner at the time.
Unfortunately, then and now, drug industry funded doctors have tried to claim that the warnings scare doctors and patients away and heighten suicide. While it would be ridiculous to blame obesity on tighter restriction of obesity drugs, that is essentially what drug industry spokesmen have done with SSRI warnings and continue to do.
Even The New York Times was misled by such disinformation, reporting that SSRI warnings were causing a leap in suicides.
Journalist Alison Bass, however, revealed14 the paper on which the Times article was based was funded by a $30,000 Pfizer grant. The conclusions about higher suicides also turned out to be wrong because the researcher got his years mixed up.15
Contrary to drug industry claims about the warnings, the proportion of children and teens taking antidepressants actually rose in the U.S. after the Black Box was added from more than 1 percent to nearly 2 percent says Dr. Andrea Cipriani, associate professor in the department of psychiatry at the University of Oxford, in England.16
Still, both David Shern, Ph.D., president of Mental Health America, a group investigated by Congress for undisclosed industry funding17 and Dr. Charles Nemeroff, also investigated by Congress, blamed18 the Black Box warnings for rising suicides. Speaking to ABC News, Nemeroff said:19
“I have no doubt that there is such a relationship. The concerns about antidepressant use in children and adolescents have paradoxically resulted in a reduction in their use, and this has contributed to increased suicide rates.”
False Charges About Black Box Warnings Continue
Nemeroff left his post at Emory University in disgrace because of his drug industry links20 and a National Institutes of Health (NIH) grant he managed was suspended because of the conflicts of interest — a rare occurrence.21 Nor have the false charges about Black Boxes died down. Here is how a New York Times editorial read just last year.22
“Worse, antidepressants, which can be lifesaving, are probably being underused in young people. Their use fell significantly after the FDA issued its so-called black-box warning in 2004, stating that all antidepressants were associated with a risk of increased suicidal feeling, thinking and behavior in adolescents. That warning was later extended to young adults.
It’s not hard to understand why. The FDA’s well-intended warning was alarming to the public and most likely discouraged many patients from taking antidepressants. Physicians, too, were anxious about the admittedly small possible risks posed by antidepressants and were probably more reluctant to prescribe them.
This very small risk of suicidal behavior posed by antidepressant treatment has always been dwarfed by the deadly risk of untreated depression … Parents and teenagers, and their doctors, too, should not be afraid of antidepressants and should know that they can be very helpful. Indeed, with careful use and monitoring, they can be lifesaving. The only thing we should all fear is depression, a natural killer that we can effectively treat.”
Blaming underuse of drugs and falling sales on warnings that made patients or doctors “anxious” is not limited to antidepressants. Recently, industry-funded groups charged that warnings on the bone drugs called bisphosphonates about fractures and osteonecrosis of the jaw were scaring patients and doctors away and denying patients the drugs’ benefits.23
SSRIs Ignored in the Extremely High Rate of Suicide in the Military
During the wars in Iraq and Afghanistan, troop suicides were higher than combat fatalities themselves and the majority of the suicides were among troops who had never even deployed.24 But when a long awaited Army report came out, it largely blamed soldiers themselves for the deaths, especially highlighting illegal drug usage and barely mentioning the huge number of troops on prescription psychoactive drugs. In fact, the word “illicit” appears 150 times in the Army report and “psychiatrist” appears twice.25
At the time of the Army report, 73,103 prescriptions for Zoloft had been dispensed to troops, 38,199 for Prozac, 17,830 for Paxil and 12,047 for Cymbalta.26 In fact 4,994 troops at Fort Bragg alone were reported to be on antidepressants by the Fayetteville Observer.
Four years after the Army report, researchers addressed the military suicides in JAMA Psychiatry27 again not finding or considering the high prescribing of SSRIs within the military. The authors had financial links to Eli Lilly, GlaxoSmithKline, Ortho-McNeil Pharmaceutical, Janssen-Cilag, Pfizer, Sanofi-Aventis, Shire and Johnson & Johnson.
In a series during the Iraq and Afghanistan wars called “Medicating the Military,” when SSRI use was mushrooming, Military Times reported:28
“A Military Times investigation of electronic records obtained from the Defense Logistics Agency shows DLA spent $1.1 billion on common psychiatric and pain medications from 2001 to 2009. It also shows that use of psychiatric medications has increased dramatically — about 76 percent overall, with some drug types more than doubling — since the start of the current wars.
Troops and military health care providers also told Military Times that these medications are being prescribed, consumed, shared and traded in combat zones — despite some restrictions on the deployment of troops using those drugs. The investigation also shows that drugs originally developed to treat bipolar disorder and schizophrenia are now commonly used to treat symptoms of post-traumatic stress disorder, such as headaches, nightmares, nervousness and fits of anger.
Such ‘off-label’ use — prescribing medications to treat conditions for which the drugs were not formally approved by the FDA — is legal and even common. But experts say the lack of proof that these treatments work for other purposes, without fully understanding side effects, raises serious concerns about whether the treatments are safe and effective.”
Many military administrators have unabashed drug company links, like Dr. Matthew Friedman, former executive director of the Veterans Affairs’ National Center for PTSD,29 who admitted receiving AstraZeneca money in a video on the Center’s site a few years ago (a video since taken down) and served as Pfizer Visiting Professor while helming a government organization.30
Recently, the Annals of Internal Medicine ran another study looking at military suicides without finding an antidepressant role. The study’s editors at the Annals had links31 to Eli Lilly, Pfizer and Johnson & Johnson. Considering all the risks associated with antidepressants, it would be wise to use them as a very last resort. To learn more about safer treatment options, please see my previous article, “Supplements Proven Beneficial for Your Mental Health.”
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Brazil’s Ministry of Health has launched an investigation into the cluster of babies born with brain defects linked to the Zika virus, after an expected “explosion” of cases across the country did not occur.
The bulk of the cases of congenital Zika syndrome – fetal brain defects that sometimes cause microcephaly, or abnormally small skulls – remain clustered in the northeast region of the country where the phenomenon was first identified last October, the ministry says.
And that has epidemiologists and infectious disease experts asking what is going on: Is it Zika and another virus working together that damages the fetal brains? Is it Zika and an environmental factor? Or something about the women themselves whose fetuses are affected?
The research in Brazil won’t have conclusions for months, but will have implications across the Americas, where the Brazilian experience and the rapid spread of Zika has caused governments to take protective measures and even warn women to delay getting pregnant.
“We can see there is a kind of cluster in [part of] the northeast region with high prevalence and high severity, of miscarriage and congenital malformation that is really severe,” said Fatima Marinho, co-ordinator of epidemiological analysis and information at the ministry.
“But we didn’t find this in other states – even the [adjacent] states didn’t see the same situation as in the epicentre…. We were preparing for an explosion and it didn’t come.
“So we started to think that in this central area maybe more than Zika is causing this intensity and severity.”
A central theory the ministry is now exploring is whether co-infection with other viruses, such as dengue or chikungunya, is the factor. For example, does a mother’s previous (or simultaneous) infection with dengue, which is also ubiquitous in Brazil, mean that the Zika virus affects a fetus differently? Or is it other viruses?
“This is an area that was under attack by viruses: Some parts even had measles,” during the period when the bulk of the congenital Zika babies were conceived, Dr. Marinho said.
The ministry is also looking at social determinants, she said, because initial analysis makes it clear the women with affected fetuses have a clear “profile.” Some 77 per cent of them are black or mixed-race (the national figure is 52 per cent), and the great majority are poor. That’s surprising, she said, given that dengue, for example, carried by the same mosquito, infects people across social classes. Most of the mothers are young (between 14 and 24) whereas typically birth defects affect older women.
The World Health Organization is supporting research into co-factors. “Even though a causal link between Zika virus and congenital malformations has been conclusively demonstrated as published in international peer-reviewed scientific publications, other factors that may aggravate these conditions also require investigation,” said Sylvain Aldighieri, incident manager for Zika with the Pan American branch of the WHO.
“I totally agree some co-factors are likely involved,” said Eduardo Marques, a professor of infectious disease and microbiology at the University of Pittsburgh and scientific director of a program called Cura Zika. But it isn’t the cluster that convinces him: “It’s because not every woman exposed during pregnancy has a baby with the congenital effects.”
But not all epidemiologists concur: “I think it’s too early to say there is a disparity in the rate of microcephaly,” said Laura Rodrigues, a professor of infectious disease epidemiology at the London School of Hygiene and Tropical Medicine, who has been working on Brazil’s Zika epidemic since it was first identified. The epidemic is nearly a year behind in its spread in some other countries and perhaps other parts of Brazil, she said. “So maybe haven’t got to the peak. But that’s not to say we shouldn’t think about co-factors.”
Because the virus produces no symptoms in up to 80 per cent of people who get it, and only mild symptoms in many others, few people confirm Zika infection with laboratory tests, and so statistics of Zika cases are always estimates. The virus currently infecting Brazilians is a new, Asian strain of Zika, which was identified more than 60 years ago but never associated with congenital problems, or known to be sexually transmissible, as this strain is.
After Brazil, the next country that was expected to see the wave of congenital Zika was Colombia, which has the second-largest number of reported Zika cases. But of more than 12,000 pregnant Colombian women with Zika, only 21 have had fetuses or babies with the brain defects.
Dr. Marinho, with the ministry, said this reinforces her suspicions about the role of co-infection or other factors in Brazil. Dr. Marques said Colombia is only seeing the babies of women who were infected late in their pregnancies so far (because the virus season is about six months behind, further to the north) and the evidence is that the likelihood of damage by Zika is higher earlier in gestation – so those babies may yet come.
But Dr. Rodrigues had another explanation. “Now we know that in places where Zika comes the rate of abortion shoots up,” she said. “The feminist groups that will send pills by post to women … as a way of making up for the unfairness of the restrictive abortion laws, report an enormous increase in requests from Brazil and Latin America. I wouldn’t be surprised if when we look at cohorts in other counties, pregnancies disappear, and we can’t say if it was spontaneous or medical abortion.”
Researchers reported in the New England Journal of Medicine on July 28 that in Latin American countries where the new strain of Zika is spreading and abortion is illegal, there has been a huge spike in the number of requests to Women on Web, a Dutch-based organization which proves women with online consultations and then mails the drugs to induce a medical abortion. The increase over the rate of requests last year ranges from 38 per cent to 108 per cent in Brazil. (Brazilian authorities are now intercepting all deliveries to Brazilian women, the group said.)
On July 15, Adriana Melo, a fetal medicine specialist in the state of Paraiba who was the first to find Zika in the brains of affected babies, released research in which she and her co-authors report finding proteins of bovine viral diarrhea virus (BVDV), a cattle disease, in the brains of three fetuses with microcephaly from Paraiba whose brains also tested positive for RNA from the Zika virus. BVDV is known to cause serious birth defects in cows, but not to infect people. The findings were posted on BioArchive, a U.S.-based website for scientists to quickly share research findings on urgent matters, before peer review and publication. Their hypothesis is that Zika infection may weaken physiological barriers, so the cow virus that would not normally affect a human fetus can cause damage.
However other researchers are expressing skepticism of this theory – and Dr. Melo and her colleagues acknowledged the possibility that the BVDV they found was the result of sample contamination, because the virus is often found in fetal bovine serum, which is a reagent (a substance used in chemical analysis) frequently used in laboratories.
Dr. Marinho is at pains to make clear that the health ministry does not doubt that Zika is the primary cause of the fetal brain damage. (Brazilian doctors were quick to persuade the ministry of the link last year, but had a much longer job to convince the World Health Organization, which declared an emergency over microcephaly only in February.) Then conspiracy theories tore through the public in Brazil and beyond – that microcephaly was actually caused by a pesticide, or vaccines, or genetically modified mosquitoes – and she does not want to revive that debate.
“We know here Zika caused neurological damage – we have no doubt – but the question is how can we explain this situation in the epicentre that was not reproduced in other areas – in Colombia, and in other states in Brazil. A lot of pregnant women were infected and there were few cases of microcephaly or congenital malformation – it must be more than Zika itself,” she said. “We could be wrong of course but it is the responsibility of the Ministry of Health to investigate all possibilities.”
Beneath all of these theories lies a fundamental problem with data. Until this crisis, Brazil had very weak reporting of microcephaly, with rates in some areas reported as 1,000 times lower than in Europe even though researchers have every reason to believe that it occurred at roughly the same rates.
With the emergency declared, health workers suddenly erred in the wrong direction, overreporting microcephaly. Almost none of the women with affected babies had a serologically confirmed Zika diagnosis. Beyond that, Dr. Melo and her colleagues realized many of the worst-affected babies had completely normal looking skulls, and it was not until they showed neurological problems that they were reported as Zika-affected. She told The Globe in February that it was impossible to know how many had slipped through the net and were as yet undiagnosed. In addition, an unknown number of affected pregnancies ended in miscarriage.
“The current epidemiological info is very fragile, so how do we know, for example, that we didn’t have an explosion of cases in Rio in 2014 and we didn’t pick it up?” asked Dr. Marques.
The Asian strain of Zika hit French Polynesia in 2013 and researchers have gone back to retrospectively diagnose 17 cases of babies born with microcephaly in a total population of 275,000 people – but researchers hotly debate how useful that information is for indicating the likelihood of co-factors, since it’s retrospective and based on modelling. In addition, while Zika was not known to be related to fetal development problems at the time, abortion is legal in French Polynesia and women who were told their babies had brain defects could have terminated their pregnancies.
Brazil has 1,749 cases of confirmed congenital Zika syndrome so far, with 106 stillbirths and deaths. Dr. Marinho said it will be months before the ministry has solid data to confirm that the cases are clustered and there are co-factors involved, let alone what they are, and meanwhile congenital Zika remains a real threat: Paraiba is now seeing a second wave of cases. “But this could be good news, for other areas of Brazil, and other countries,” she said.
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In a puzzling case, a person in Utah became infected with the Zika virus, but health officials can’t figure out how the person contracted it.
The infected person was a caregiver for an elderly man who had Zika. But the case is mysterious: As far as health officials can tell, the caregiver wasn’t exposed to Zika in a way that would transmit the virus, at least from what’s currently known about Zika. So far, the only way Zika was thought to spread from person to person is through sexual contact, and the caregiver did not have sexual contact with anyone who had Zika.
“Zika continues to surprise us,” and there’s still a lot we don’t know about the virus, Dr. Satish Pillai, incident manager for the Centers for Disease Control and Prevention’s Zika response, said at a news conference today (July 18). [Zika Virus News: Complete Coverage of the 2016 Outbreak]
Health officials are currently investigating how the caregiver could have caught the virus, including whether Zika could be passed from person to person in special situations, even if the situation does not involve sexual contact.
“We’re still doing a lot of investigation to determine whether Zika can be spread from person to person through contact with a sick person,” Pillai said.
But the health officials stressed that the primary way that Zika is spread is through bites from mosquitoes that carry the virus. Of the more than 1,300 cases of Zika in the United States, nearly all involve people who caught the virus while traveling in an area where Zika is spreading. Fourteen people in the United States have now caught the virus through sexual transmission, and one person caught Zika while working with the virus in the laboratory.
“We don’t have evidence right now that Zika can be passed from one person to another from sneezing or coughing,” or from other types of casual contact, such as touching or sharing utensils, Pillai said.
The caregiver in the Utah case had not traveled to an area where the Zika virus is spreading, and mosquitoes that spread Zika have not been found in Utah.
But the person did take care of an elderly man who caught Zika virus while traveling to another country. The elderly man later died, although it’s not clear if he died from Zika or another underlying condition, officials said.
There was an unusual aspect of the elderly man’s case: He had extremely high levels of the Zika virus in his blood before he died — more than 100,000 times higher than the levels seen in other people infected with the virus so far, officials said.
“This is a very unique situation,” with such high levels of the virus, Pillai said. But researchers still don’t know whether this high level of the virus played a role in how the man’s caregiver caught Zika.
Health officials are currently interviewing the newly infected person and the person’s family members to learn more about the types of contact the caregiver had with the elderly man, according to the Utah Department of Health.
The caregiver showed mild symptoms of Zika, and has since recovered from the infection, officials said
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TUESDAY, March 22, 2016 (HealthDay News) — Do you get a moderate amount of exercise, eat right, keep from piling on fat and avoid smoking? Congratulations, you’re among the 2.7 percent of Americans who do so, according to a new study.
Researchers say that, unfortunately, the other 97.3 percent of American adults get a failing grade on healthy lifestyle habits.
“The behavior standards we were measuring for were pretty reasonable, not super high. We weren’t looking for marathon runners,” said study senior author Ellen Smit, an associate professor at the OSU College of Public Health and Human Sciences, in Corvallis.
In fact, the standards used in the study are typical of lifestyle advice given by doctors to their patients, Smit’s team said. People who adhere to those four behaviors can help reduce their risk of many health problems, including type 2 diabetes, heart disease and cancer.
Unfortunately, less than 3 percent of the adults in the study achieved all four of the healthy living measures, the researchers found.
Overall, 71 percent of the adults surveyed did not smoke, 38 percent ate a healthy diet, 10 percent had a normal body fat percentage and 46 percent got sufficient amounts of physical activity.
Sixteen percent had three of the healthy lifestyle behaviors, 37 percent had two, 34 percent had one and 11 percent had none.
Among the other findings: women were more likely than men to not smoke and to eat a healthy diet, but they were less likely to have adequate physical activity levels. And when it came to race, Mexican-Americans were more likely to eat a healthy diet than blacks or whites.
The study was conducted by researchers at Oregon State University, the University of Mississippi and the University of Tennessee-Chattanooga.
In terms of public health, the findings are disappointing, Smit said in an OSU news release.
“This is pretty low, to have so few people maintaining what we would consider a healthy lifestyle,” she said. “This is sort of mind boggling. There’s clearly a lot of room for improvement.”
Further research is needed to identify ways to get American adults to adopt more healthy lifestyle habits, the experts said.
The study was published recently in the journal Mayo Clinic Proceedings.
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When it comes to obtaining sufficient amounts of certain micronutrients, you’re hyper vigilant. Magnesium? You’re eating spinach, throwing back magnesium glycinate, and adding Trace Mineral drops to your water. Iodine? You’re making dulse “bacon.” To bask in the holy triumvirate of vitamin K2, vitamin D3, and vitamin A, you’re willing to eat fermented cod liver oil and stinky natto. But as omnivores drawing upon a broad spectrum of plant and animal foods, Primal people tend to assume they have the B vitamins covered. It’s no wonder: punch a slab of beef chuck steak or a few ounces of liver into the USDA nutrient database and that whole B vitamin section seems to fill up.
Let’s take a look. You may be right. You may be totally fine. But it’s always nice to refresh your focus.
Vitamin B-1 (Thiamine)
Thiamine is a co-enzyme used to produce ATP, the energy currency of the body. Without adequate thiamine, your power levels drop. Wouldn’t want to be low energy, would you?
- Serious thiamine deficiency leads to an often-fatal condition that affects the cardiovascular system called beriberi. This is hard to get in developed countries, or any country that fortifies its grains. “Dry beriberi” is another serious condition that affects the nervous system.
- Carbohydrate intolerance. Thiamine, which helps regulate glucose metabolism, has a strong connection to diabetes. Diabetics consistently have low serum levels of thiamine and the severity of diabetic symptoms matches blood thiamine.
- Fatigue, listlessness, brain fog.
- Poor sleep (thiamine is a co-factor in GABA production).
Why Might Deficiency Occur?
- Avoidance of fortified grains. Most people get adequate thiamine because they’re eating diets based on refined white flour, which is fortified with the vitamin. I don’t advise this tactic, but it does work if all you care about is thiamine. Primal eaters will have to eat other stuff.
- Excessive alcohol consumption, which impairs thiamine absorption and increases thiamine utilization.
Where to Get It
- Although most health websites never mention it, pork is the single best dietary source of thiamine. It’s in the muscle meat, so any amount of lean pork will be rich in thiamine. You don’t need much, either. 100 grams of lean pork gets you almost all your daily thiamine (PDF).
- After pork, various seeds (sunflower, in particular) and veggies (spinach, asparagus) are good sources.
- Supplement. Thiamine HCL is a common, well-tolerated form.
Men need about 1.3 mg per day, women 1.2 (1.4 when pregnant or breastfeeding). High-dose thiamine (300 mg/day) is safe and has been used to improve glucose tolerance, fatigue after stroke, fatigue in multiple sclerosis, and fatigue in inflammatory bowel disease. In young women with adequate thiamine status, 50 mg/day improved reaction time.
Vitamin B-2 (Riboflavin)
Riboflavin is a facilitator; it helps activate other B-vitamins like folate, thiamin, and B-12. It’s also a necessary co-factor in glutathione recycling.
- Cracked lips and skin, throat swelling and soreness, swollen tongue, scaly skin.
- Pre-eclampsia. Pregnant women deficient in riboflavin are almost 5 times more likely to develop pre-eclampsia than replete women.
- Low niacin. Riboflavin enables the conversion of tryptophan to niacin.
- Anemia. Adding riboflavin to an iron-folate supplement combats anemia better than iron-folate alone.
- High homocysteine. Certain MTHFR mutations increase the need for riboflavin.
Why Might Deficiency Occur?
- Poor diet. Riboflavin is present in many foods, but a monotonous, limited diet can run short.
Where to Get It
- Liver, dairy, meat, nuts, eggs, green vegetables.
- Supplement. It just goes by riboflavin or vitamin B-2.
1.3 mg/day for men, 1.2 mg/day for women. Excess riboflavin is excreted in the urine, turning it yellow.
Vitamin B-3 (Niacin)
Like every other B vitamin, niacin figures prominently in the energy generation process, particularly the glucose-to-ATP pathway.
- Pellagra is a fatal condition caused by gross niacin deficiency. It doesn’t happen much anymore with widespread food fortification.
- Elevated blood lipids. Taking niacin can raise HDL and lower the total/HDL ratio. It even beats statins when it comes to improving blood lipids and lowering arterial plaque.
- Low appetite.
Why Might Deficiency Occur?
- Too much alcohol.
- Insufficient intake of animal foods. Not only are animal foods the best source of niacin, they’re also the best source of tryptophan, which our bodies can convert to niacin when needed. This is actually why food fortification was enacted—to make up for the lack of animal foods in many nations’ diets.
Where to Get It
- Fish, especially tuna, is the single best source, followed by beef liver, pork, dairy, and poultry. Mushrooms and sunflower seeds aren’t too shabby, either.
- Supplement. Niacin often causes unpleasant facial flushing—that’s how you know it’s working. Older sustained release forms of the vitamin eliminated the flushing but didn’t work as well and caused other, more dangerous side effects, like liver damage. Both instant release niacin and newer extended release niacin appear to be safe and effective at reducing cardiovascular disease, so stick with that if you’re trying to prevent heart disease. High-dose niacin of any type is more drug-like than vitamin-like, so be sure to consult a medical professional.
16 mg/day for men, 14 mg/day for women. Higher levels are safe if you can handle the flushing.
Vitamin B-4 (Choline)
Originally classified as the 4th B vitamin, choline was downgraded, but I don’t buy it. Choline is incredibly important for liver and brain health, and people aren’t eating the egg yolks and liver that provide the biggest doses of it like they once did.
- Fatty liver: Without enough choline to process the fats entering it, the liver may begin to store visceral fat.
- All the downstream effects of fatty liver, including insulin resistance, type 2 diabetes, cardiovascular disease, and, eventually, eternal damnation.
- Brain fog, memory deficits, general mental “bleh”ness. Choline begets acetylcholine, an important neurotransmitter. Remember how a ton of nootropics purport to act via acetylcholine pathways? Choline’s the currency.
Why Might Deficiency Occur?
- Liver insults: Any insult to the liver, like alcohol consumption, increases the amount of choline you need.
- High-fat diet: Higher fat intakes require more choline to process the fat.
- Pregnancy and lactation: Not a true deficiency, but as choline helps build baby brains and gets diverted to breast milk, both pregnancy and breastfeeding increase choline requirements.
- Not enough egg yolks and liver.
- Inadequate folate intake: Folate is required to metabolize choline.
Where to Get It
- Egg yolks (120 mg/yolk), liver (426 mg/100 g), kidney (513 mg/100 g), brain (491 mg/100 g), fish roe (335 mg/100 g).
- Supplement. Lecithin, choline bitartrate (41% choline by weight), alpha-GPC (40% choline by weight) are all different types of choline.
550 mg for men and pregnant women, 450 mg for women.
Vitamin B-5 (Pantothenic acid)
Pantothenic acid is present in most foods, so deficiency is really hard to attain. That doesn’t negate its importance in dozens of physiological processes.
- Tingling and numbness in the extremities, intestinal upset, headaches, fatigue. Again, almost unheard of in humans with access to food.
- While outright deficiency is hard to achieve, extra B-5 may prove useful for people with acne (some researchers even think pantothenic acid deficiency presents as acne).
Why Might Deficiency Occur?
- Pantothenic acid is used in ethanol metabolism, so anyone drinking alcohol would be well-served with a dose or two.
- Complete and utter starvation. An all-olive oil diet (olive oil is one of the few foods without B-5).
Where to Get It
- All plant and animal foods (except for pure oils; pantothenic acid is water-soluble). Sweet potato, avocado, and mushrooms top the list of plant foods. Organ meats, shellfish, eggs, fish, and dairy top the list of animal foods.
- Gut bacteria manufacture pantothenic acid, which may be absorbed by the host.
- Supplement. Calcium pantothenate is the standard effective form.
There is no upper limit set for pantothenic acid, a strong indicator of its innocuousness.
Vitamin B-6 (Pyridoxine)
B-6 is a co-factor in dozens of enzymatic reactions, including the synthesis of neurotransmitters and creation of proteins (like tryptophan).
- Morning sickness. Studies indicate that B-6 supplementation can reduce pregnancy nausea.
- Inflammation. Elevated CRP is more likely in people eating less than 2 mg of B-6 a day.
Why Might Deficiency Occur?
- Pregnancy increases B-6 requirements.
- Long-term use of medications, including oral contraceptives and NSAIDs. Both may impair B-6 metabolism or distribution.
- Low B-6 intake. It’s present in a lot of foods, but not all of them.
Where to Get It
- Potatoes, bananas, poultry, nuts, fish, and legumes.
- Supplement. B-6 is widely available and inexpensive.
Aim for about 2 mg a day. Long term mega doses (1000 mg/day) may cause sensory neuropathy, characterized by numbness, pain, and difficulty walking.
Vitamin B-7 (Biotin)
Another fallen B-vitamin, biotin is everywhere. We can’t make it from scratch, but our gut bacteria make it for us, it’s present in many foods in our diet, and our bodies can even recycle the biotin we’ve already used for later use.
- Weak, brittle nails. Biotin supplementation may improve nail strength.
- Progressive multiple sclerosis (maybe). A recent pilot study found that high dose (100-300 mg a day with the recommended normal intake being just 30 micrograms) biotin supplementation helped to stop and even improve the progression of multiple sclerosis. More research is underway.
Why Might Deficiency Occur?
- Biotinidase deficiency, a hereditary condition which prevents biotin from being recycled from proteins in the body or absorbed from foods. Standard newborn screening usually looks for this, and biotin supplementation effectively treats it.
- Too many raw egg whites. Uncooked egg whites contain avidin, which binds to biotin and reduces absorption.
- Dairy allergy. Dairy is a common, reliable source of biotin, and some studies have shown biotin deficiency to be common in kids with milk allergy.
- Broad spectrum antibiotics can disrupt the bacteria that make biotin.
Where to Get It
- It’s all over, but the best sources are eggs, dairy, organ meats, avocado, pork, chicken, broccoli, cauliflower, and spinach.
- Supplement. Look for biotin.
30 micrograms per day for all adults. More for pregnant women.
Vitamin B-9 (Folate)
Folate is a big one. It’s required for DNA methylation (a key component of gene expression) and synthesis of vital amino acids like methionine. Basically, if you want all the genes in your body to work and produce the proteins they’re meant to produce, you need folate.
- High homocysteine. Since folate converts homocysteine into methionine, folate deficiency usually leads to excess homocysteine.
- Neural tube defects in offspring. This ins’t a true symptom since you won’t notice until it’s too late. Prenatal supplementation of folate (or an emphasis on folate-rich foods before and during pregnancy) is crucial.
Why Might Deficiency Occur?
- MTHFR mutations which increase requirements and impair metabolism.
- Insufficient intake of folate-rich foods, especially if you’re avoiding fortified grains (which most of you probably are). See below for a list.
- Lack of vitamin C in the diet. Vitamin C improves folate absorption.
Where to Get It
- Chicken liver is the single best source of folate followed by other livers. Leafy greens, pastured eggs, asparagus, lentils, and chickpeas are also good.
- Supplement. Folic acid is the most common form, but people with MTHFR mutations which impair the conversion of folic acid to folate should take folate
At least 400 micrograms a day for both men and women. 600-800 if pregnant.
According to Chris Kresser, vitamin B12 deficiency is quite common, even among those who eat plenty of the richest source of B12: animals.
- Unwanted weight loss.
- Dementia/Alzheimer’s-like symptoms.
- Anxiety and depression.
- Autism spectrum disorder in children.
Why Might Deficiency Occur?
- We aren’t looking for it. As meat-eaters, we assume we’re getting plenty, and doctors don’t check for it regularly.
- We aren’t absorbing the B12 in our food. Gut disorders like Crohn’s or diarrhea affect our ability to absorb nutrients, minerals, and vitamins, including vitamin B12.
- We set the bar for “normal” too low. Everything could check out and look fine on paper, but the lower end of “normal” is too low and can still cause B12 deficiency symptoms. Other countries, like Japan, have higher “normal” B12 markers and fewer cases of Alzheimer’s/dementia.
Where to Get It
- Animals. Liver, sardines, and salmon rank highest, with liver running away with it. There are no vegetarian sources.
- Supplements. Methylcobalamin is probably the best.
If you eat animal products regularly and liver occasionally, you’ll be getting plenty of B12 in your diet. No need to supplement if you have none of the symptoms listed above. But if you have some of the symptoms, or you have a gastrointestinal disorder that may be compromising your ability to absorb vitamin B12, consider getting your levels tested during your next visit to the doctor. In that case, try 1 mg/day of sublingual methylcobalamin, which will bypass the intestinal tract and pass directly into the bloodstream.
Should you supplement?
Not everyone needs to supplement. I’d say most people reading this don’t need to supplement.
Pregnant women usually need more of everything, and the B vitamins are no exception. Standouts for pregnant ladies include B12, choline, and folate. Any decent prenatal supplement will provide ample B vitamins.
People with depression may want to throw in a B-complex, which has been shown to improve depressive symptoms across all groups (severely depressed, mildly depressed, people without clinical depression) and increase B-12 and folate status. The involvement of various B vitamins in energy generation, neurotransmitter production, antioxidant capacity, and vitamin activation suggest it’s just a good idea for depressive patients to be replete.
Heavy drinkers should probably take more B vitamins, as ethanol metabolism depletes pretty much all of them.
One way to determine your needs is to go through the list of symptoms and see what applies to you.
Another is to get your serum levels tested, particularly if you suspect a deficiency.
But seriously, folks: just eat a quarter to a half pound of ruminant liver every week. It’s the best way to ensure you’re eating adequate amounts of practically every B vitamin you need. That little dose of liver combined with an overall healthy diet rich in animal products, leafy greens, nuts, mushrooms, and other foods mentioned in the vitamin profiles from today’s post will provide plenty.
Thanks for reading, everyone, and I hope today’s post was informative!
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For many, the morning cup of coffee is a can’t live without ritual. There are studies that show moderated daily coffee is healthy for you (some of that here). For me, it kind of makes me shaky. I drink it few and far between. That’s a personal thing, of course. However, when I do drink it, I always put butter in it. As weird as it sounds, it’s actually the best thing you can put in your coffee.
When I get in line at Starbucks, I order a plain black coffee and ask them for a side of butter. They give me some pretty odd looks, but what I already know is that every Starbucks has butter packets on hand to go along with their oatmeal. And what’s more? It’s Kerrygold Irish butter. And that’s grass fed.
So what health benefit would one get from this?
Coffee can be a starting point for health, but it can also be an ending point just as easily. People order / make their coffee in all shapes and sizes. Some people add sugar laden creamers or hormone laced milk. While others might just add a little cinnamon. Those concoctions offer vastly different health profiles. Having just sugar and caffeine first thing in the morning sets up impending doom for the rest of your day. You are almost sure to crash out at some point, only to find yourself digging around for candy or a muffin.
The first health benefit you get from putting only butter in your coffee is that you are leaving out the bad stuff. A huge part of a healthy lifestyle is what you don’t eat. The butter is a fat, which will also help blunt blood sugar spikes.
Butter is almost a pure fat. That’s going to scare a lot of you, but really, it shouldn’t. Fat is good (mostly). And the idea that fat is a villain has been almost entirely debunked at this juncture. Saturated fats can actually improve your blood lipid profile (here).
Grass fed butter is loaded with Vitamin K. Wait, what? Vitamin K is awesome. And it’s sure great for the heart. There is K1 (phylloquinone), found in leafy greens, and Vitamin K2 (menaquinone), which is found in animal foods. Vitamin K2 is especially important because it helps keep calcium out of your arteries.
So far, what do we have? Putting butter in your coffee means skipping garbage sugary or hormone laced concoctions. Your arteries are less likely to be subject to calcification. You reduce your risk of coronary heart disease (here).
But hold up, its going to get better.
Person drinking coffee with butter in it…..meet Butyrate. Butyrate is a fatty acid and it is anti-inflammatory. Inflammation is pretty much the cause of all evil in the body. When excessive inflammation lurks, so does bad healthy profiles. Butyrate is shown to lower inflammation (here).
CLA (conjugated linoleic acid) is found in grass fed butter and it has been linked to reducing body fat mass. Yep, your old coffee was plumping you up, your new coffee is slimming you down! You can see a study here.
But how gross does it taste?
I get this question all the time. The answer is that it taste great. And no, I’m not just saying that. You have to stop thinking of it as butter, and start understanding that at the end of the day, it is just heavy cream. If you put butter and cinnamon in your coffee, it taste amazing. Now, again, we are talking grass fed butter here, not just any old butter. The most popular is Kerrygold butter, but if you have a store that sells local products you can likely find whatever suits you.
The point in all of this? Your morning coffee can be a true health bomb!
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The proverbial brick wall of bad dietary advice is a-crumblin’. This week brings truly world-changing news in the field of nutrition.
On May 8, the Academy of Nutrition and Dietetics (formerly the American Dietetic Association) made its official comments on the 2015 Dietary Guidelines for Americans, and recommend dropping saturated fat from nutrients of concern due to the lack of evidence connecting it with cardiovascular disease.
However, because past advice from the Academy and others has caused issues with ALL of our body systems, I would also argue that this is actually earth-shattering news in the world of cardiology, nephrology, lipidology, endocrinology, pulmonology, orthopedics…. you get the point.
The Academy supported the scientific process used by the Dietary Guidelines Advisory Committee (DGAC) in drafting its recommendations for the 2015 Dietary Guidelines for Americans, but had somewhat different interpretations:
- They supported the DGAC in its decision to drop dietary cholesterol from the nutrients of concern list and recommended that it also drop saturated fat from nutrients of concern, citing a lack of evidence connecting saturated fat with cardiovascular disease;
- Expressed concern over blanket sodium (salt) restriction recommendations in light of recent evidence of potential harm to the larger population;
- Supported an increased focus on reduction of added sugars as a key public health concern; and
- Asserted that enhanced nutrition education is critical to any effective implementation.
Why is all of this so earth-shattering? Well, it brings an end to the era of jumping to conclusions and issuing recommendations before we had the science. It brings an end to a big experiment on the American people and, by extension, the rest of the world, which has failed miserably. It is an acknowledgment that the recommendations to restrict fat, most particularly saturated fat, which led to the recommendation to eat more than half of our energy intake EVERY day from carbohydrates was…WRONG! Yes, the food pyramid, eating sugared cardboard products and highly processed vegetable oil instead of real foods like meat and eggs were all just, I have to say it again, plain WRONG.
As an obesity physician who sees the fallout from the previous guidelines in the poor health of my patients every day, I am thrilled. I am thrilled because this means that more people will be helped. More people can realize that much of the reason that they are obese, have diabetes, high cholesterol, or metabolic syndrome is NOT all their fault. Yes, I really just said that. (What? Not blame a fat person for being fat? Uh, exactly. )
This is not news for the community of bariatrics physicians. We knew that fat was not the cause of the disease we treat nor for the related diseases, such as diabetes or metabolic syndrome. In fact, when the U.S. Department of Agriculture and later the American Dietetic Association (now the Academy of Nutrition and Dietetics) began recommending reducing fat and pushing an increased intake of carbs was exactly the years when our obesity and diabetes epidemic began. Just a correlation? We have much reason to think it is far more than correlation and is actually the cause.
That’s why in a recent TEDx Purdue talk I gave it the title “Reversing Type 2 diabetes starts with ignoring the guidelines.” The guidelines have been misguided for years, and work against patients with obesity, Type 2 diabetes, or metabolic syndrome.
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“Essential minerals” – what are they?
The word “minerals” means different things in different sciences. In geology, ‘minerals’ are chemical compounds that are not made by biological organisms – quartz would be an example. In biology, however, the word “mineral” refers to chemical elements, (not chemical compounds) – any element except hydrogen, carbon, nitrogen, and oxygen (which are considered too ‘organic’ to be called minerals).
An “essential mineral” is a mineral that is required by organisms for survival or at least for health. Thus, the essential minerals include the elements calcium, chlorine, chromium, cobalt, copper, iodine, iron, magnesium, manganese, molybdenum, phosphorus, potassium, selenium, silicon, sodium, sulfur, and zinc. The elements boron, nickel, tin, and vanadium are also suspected to be essential minerals. Proponents of germanium supplements claim that germanium is an essential mineral, too, but there is not yet enough evidence to include it in the list.
The essential minerals (which now we’ll just call ‘minerals’) play fundamental roles in all living organisms. Many of them are active parts of enzymes that perform chemical conversions – for example, the sugar-metabolizing enzyme Cytochrome C Oxidase contains copper and iron atoms. Other minerals are structural components of certain tissues – such as silicon, which strengthens connective tissue and nails. Still others serve as regulators and signallers – as with potassium, which is involved in controlling the activity of nerve cells.
Bioavailability of minerals
Minerals enter the body mostly as components of food. But elemental minerals (such as sulfur in the form of yellow sulfur crystals), are generally not bioavailable. To become bioavailable, mineral atoms must be combined with other elements to form chemical compounds. For example, most of the body’s sulfur comes from sulfur-containing amino acids in food proteins. Similarly, the body gets most of its manganese not from nodules of manganese metal, but from manganese-containing substances in food – that is, from plant and animal tissues in which the manganese is already incorporated into enzymes similar to those that our own bodies will make from it.
There is thus a great deal of mineral recycling going on in the biosphere: mineral compounds travel from one organism to another when the latter eats the former. But not all of the minerals found in biological organisms are the result of such recycling of mineral compounds. Some minerals enter the biological world when elemental minerals (such as manganese metal) are converted to chemical compounds (such as manganese carbonate) in the soil or elsewhere – the result both of non-biological chemical reactions and of conversions by bacteria and other microorganisms. As elemental minerals get converted to mineral compounds, these simple inorganic compounds become bioavailable to plants. The plants then perform the conversion to more complex organo-mineral compounds (such as manganese-containing enzymes) which makes them bioavailable to other organisms – to animals, for example.
Transport of minerals into cells
When mineral compounds are consumed in food, the body must somehow absorb the minerals from the digestive tract and make them available to the tissues and cells where they are needed. The process is not a simple one. The minerals cannot simply diffuse into our tissues and through cell membranes into the interior of cells – if they could, their concentrations would fluctuate in accordance with whatever amounts of minerals we happen to consume at any given time. Instead, the mineral-containing compounds (or charged mineral atoms taken from these compounds) are transported into (or out of) cells by transporter proteins – molecular devices embedded in cell membranes that recognize the minerals and allow only certain kinds to pass through the membranes. This system permits cells and tissues to regulate their internal concentrations of minerals.
Looked at from an engineer’s viewpoint, an organism’s mineral transport system serves as a regulatory device for maintaining adequate, but non-toxic, levels of mineral atoms inside cells.
The number of different kinds of transporter proteins present in a single organism is amazing. In plants, for example, there are many hundreds of different transporter types, each specialized for certain minerals, for certain tissues, and for certain conditions. Some transporters perform only “export” operations (that is, they allow certain minerals to leave the cell but not to enter it). Others are ‘importers’. Each is regulated by the conditions around it as well as by signals coming from inside or outside the cell.
Despite the large number of different transport types, a given transporter does not necessarily have the ability to specialize in a single mineral. While each transport protein seems to have a certain mineral it ‘prefers’ to transport, many of them handle additional minerals to a lesser degree. This overlap in functionality can be thought of as ‘crosstalk’ (as in a poor-quality telephone cable that allows the leakage of information between phone lines).
The system of transporter proteins and their regulation is now the focus of intense research, and rapid progress is being made in understanding it. One fact that becomes ever clearer is that the system is extremely complex. Absurdly complex, in fact – like many of the other systems found in nature.
Much of the molecular complexity in living organisms resulted not from necessity but merely from the fact that organisms develop by evolution, not by design. Evolution does not produce elegant or well-designed organisms, it produces organisms whose ancestors managed to survive even in the worst of times. Survival doesn’t require elegance – it requires adequacy, redundancy and luck. The need for redundancy gives rise to organisms that resemble Rube Goldberg machines – a mish-mash of subsystems interacting in ways that any sane designer would take to be a joke.
Consequently, the mineral transport systems we find in nature seldom break down completely, but they never work in an optimum fashion. And they do not lend themselves to simple fixes or enhancements.
The complexity of this system of natural mineral transporters is unfortunate from our standpoint. Although its multiplicity of parts with overlapping functions makes it less likely to fail completely when some of the parts are defective (as they always are), this multiplicity also makes the transport system resistant to improvement. An elegant and well-designed mineral transport system would be one with a relatively small number of different transporters, each completely specialized with respect to minerals, the direction of transport, and the range of conditions under which it operates. Such a system would be relatively easy to enhance: for example, if one wished to enhance a particular type of vanadium transport, one might develop an inhibitor for the old vanadium transporter and develop an artificial vanadium transporter with desired properties, and supply the two together to the body as a combination treatment. But the natural mineral transport system would foil such an intervention: any inhibitor we might develop for one transporter would quite likely affect other transporters as well, since there is so much overlap in their functionality. And the effects of the artificial vanadium transporter would be partially nullified by regulatory responses of the natural transporter system.
Nevertheless, attempts have been made to develop artificial transporters that override the natural ones. No attempt is made to inhibit any of the natural transporters – instead, the intention is to overwhelm them by transporting minerals into cells faster than the natural transporters can get rid of them. This approach has led to the development of several simple artificial transporters which have been used with some success for certain kinds of biological enhancement. Three such artificial transporters are: 2-aminoethylphosphonic acid (AEP), aspartic acid, and orotic acid. They are “artificial” only in the sense that in biological organisms they ordinarily play roles other than that of mineral transporters. Specifically, orotic acid is used in the biosynthesis of DNA and RNA. Aspartic acid is an amino acid that is incorporated into proteins. As for AEP, almost nothing is known about its natural role, and very little effort has been made to find out.
These three artificial transporters have become well-known in the nutritional supplement world because of the work of Hans Nieper, M.D., who studied them clinically for many years. Of the three transporters, Nieper considered orotic acid to be the most useful. He and his collaborators developed a variety of mineral derivatives of orotic acid, of which five are currently available as nutritional supplements in some countries, including Germany and the United States. These are: calcium orotate, lithium orotate, magnesium orotate, potassium orotate, and zinc orotate.
Crude tools are better than none at all
The above survey of mineral transporters should have made it clear that our current technology for enhancing the role of minerals in our bodies is still quite primitive. We have available, as mineral supplements, a few ‘artificial’ transporters that are capable of overriding the natural transporters in some situations, but which lack any regulatory features of their own. The natural transporter system, on the other hand, while overflowing with regulatory features, lacks the basic separation of functions one would find in a rationally designed system. Natural transporters evolved without any consideration of human interests or desires – basic survival was all that counted. Both sets of transporters can therefore be considered highly flawed.
Considering the fact that natural transporters at least have a track record of seeing our ancestors through some very bad times, whereas the new artificial transporters have only their brute force capabilities to their credit, is it sensible to use these crude new tools to enhance the old ones? The answer is “yes”. It makes as much sense as using any other biomedical technology of the early 21st Century – all of it is primitive, but it’s the best we have. Despite the ridiculous statements one sometimes hears – to the effect that “the human body is Nature’s masterpiece” – the fact is that, like other living organisms, the human body is a ramshackle construction that barely works even when we’re young and healthy, and fails us completely in the long run. We should therefore seek out and utilize methods for controlling or improving the way our bodies work – with appropriate caution and attention to unintended side effects. After all, we know what happens when we rely on our unenhanced bodies: our health deteriorates, we grow decrepit, and we die. Only by making use of the tools that we discover and develop will we have any chance at all of avoiding this fate.
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There are several categories of what I’ll call ‘artificial mineral transporters’ – that is, substances that are employed to enhance the passage of minerals through the intestinal wall into the blood, from the blood into the tissues, or through cell membranes into cells. (See the article Mineral transport.) Among these transporters are: colloids, amino acid chelates, carbohydrate chelates, plant chelates, and organic salts. In addition, I’ll discuss a category called ‘inorganic salts’ which are neither artificial nor transporters, but are simply a form in which minerals often occur in foods. We’ll take a brief look at each of these types.
These are simple mineral compounds such as magnesium sulfate or potassium chloride. (Carbonates, such as lithium carbonate, are usually classified as inorganic salts, although it would be more logical to consider them organic.) The body is accustomed to dealing with minerals in this form, but doesn’t always do a good job of controlling absorption. Although mineral absorption increases when there is a mineral shortage, and decreases when mineral levels are high, the body’s mineral transport system often misregulates minerals that share the same transport channels. For example, when copper and zinc salts are consumed together, they compete with each other for transport into the body. An excess of zinc can therefore cause a deficiency of copper.
If one’s purpose in using mineral supplements is to force the body to use more minerals than it normally would, the inorganic salts would be a poor choice.
Colloids are materials made up of solid particles of such small size that when dispersed in water they remain in suspension rather than sinking. “Colloidal mineral” supplements consist of mineral salts or other mineral compounds converted into colloidal form, either by grinding or by rapid crystallization.
Most colloidal substances are poorly bioavailable, since the colloidal particles, small as they are, are nevertheless far too large to be intestinally absorbed whole, and nearly all of the active ingredients are trapped in the interior of the particles, where they cannot come into contact with the transport channels in the cells of the gut. However, if a colloidal substance can dissolve into the coating of the gut, it would then release all of its mineral material for potential absorption. At this point, the material would no longer be a colloid and its absorption characteristics would become those of its components – i.e., inorganic salts, chelates, or whatever.
The word ‘chelator’ refers to a substance consisting of molecules that bind tightly to metal atoms, thus forcing the metal atoms to go wherever the chelator goes. The bound pair – chelator plus metal atom – is called a ‘chelate’. Chelators of nutritional interest include amino acids, organic acids, proteins, and occasionally more complicated chemicals found in plants.
One particular chelator that we specifically want to exclude from this discussion is EDTA (EthyleneDiamineTetraacetic Acid), which is used in a controversial treatment called “Chelation Therapy”. It involves injections of EDTA into the blood to remove (often imaginary) metallic “toxins”.
We are interested here in chelators that are intended to carry mineral atoms into the body, or into the cells themselves, in larger amounts than the body would normally allow. It is proposed that the chelators are treated as desirable molecules by the recognition systems in cell walls, and are therefore given entry into the cells, along with their baggage of mineral-atoms. When this process occurs in the cells lining the digestive tract, the minerals gain entry to the bloodstream; when it occurs in the cells lining the blood vessels, the minerals gain entry to other body tissues.
Amino acid chelates
Amino acids have three basic parts: the amino ‘group’ (i.e., group of atoms), the acid group, and the R-group. It is the R-group that determines the name and specific character of an amino acid – determining, for example, whether the amino acid is aspartic acid or lysine or tryptophan.
Amino acids can act as chelators when they react with positively charged metal atoms, forming a strong chemical bond. The metal atoms of interest here are those that serve as dietary minerals. (These are listed in the article List of dietary minerals.) To take a specific example, a chelate can be formed between the amino acid arginine (the chelator) and zinc (the mineral).
Certain combinations of minerals and amino acids do not form good chelates because the chemical bonding is too weak. For example, if you try to use the amino acid glutamic acid as chelator and sodium as the mineral, you can get monosodium glutamate, which is considered to be merely an “organic salt”, not a chelate. Monosodium glutamate undoubtedly exhibits some small degree of chelation, but this is outweighed by its character as a salt. Generally speaking, sodium and potassium form poor chelates.
Many minerals form good chelates with amino acids. Some, like lead and cadmium, have no known function in the body and are considered purely toxic. Others can be toxic in high concentrations, but are required by the body in lesser amounts. The latter include: boron, calcium, chromium, cobalt, copper, iron, magnesium, manganese, molybdenum, nickel, tin, vanadium, and zinc.
The argument in favor of using amino-acid-chelated minerals goes like this:
The body is very efficient at absorbing amino acids. Dipeptides (two amino acids linked together via the amino group of one amino acid and the acid group of the other) are especially well absorbed thanks to a dedicated transport system found in cells of the intestinal wall. When mineral atoms are strongly bonded (i.e., chelated) to dipeptides they get dragged by the dipeptides across the intestinal lining and into the body.
Furthermore, amino-acid chelation bypasses the competitive interactions that can occur between different minerals when they are absorbed as salts. (See the “Inorganic salts” section above.) Use of chelated minerals avoids this problem since they are transported by different mechanisms.
How valid is this argument? It’s hard to say, since very little published, impartial research has been done. Albion Laboratories, Inc. – the leading producer of amino-acid chelates – has sponsored many studies of its products, but these cannot be considered impartial. However, the case for amino-acid chelators of iron is a good one and is supported by a number of independent studies. The situation is less clear for other minerals. On the other hand, Albion’s products are widely used for animal and plant nutrition, and that says a lot for these substances, since farmers tend to be pragmatic and are not easily fooled about the health of their crops and animals. It seems likely, therefore, that amino-acid chelates can effectively override the normal mineral regulatory mechanisms both in plants and animals, including humans. (Albion, incidentally, has an excellent collection of research newsletters that focus on medical, veterinary and agricultural usage of minerals.)
This category of chelates is based on a large number of chelators which are called ‘organic acids’. A partial list of the organic acid chelators of interest in nutrition would include: gluconate, lactate, citrate, erythorbate, oxalate, saccharate, succinate, fumarate, 2-aminoethylphosphonate (AEP), picolinate, and orotate. (Grammatical note: chemical names ending in ‘-ate’ can equally well be expressed as ‘-ic acid salt’. For example, ‘zinc lactate’ is the same thing as ‘lactic acid salt of zinc’ or ‘zinc salt of lactic acid’.)
These chelators are called ‘organic acids’ because they are substances found in living organisms and they contain carbon atoms. The bond that forms between organic acids and mineral atoms is a relatively weak one, and is called a ‘salt bond’ or ‘electrostatic bond’. This means that the mineral atom can easily be pulled from the chelator by another molecule (such as a water molecule), or they can be separated by random jostling. Since the purpose of mineral chelation is to cause the mineral atoms to accompany the chelators through cell membranes (i.e., through the walls of the intestines, blood vessels, or other tissues), the organic acids perform only moderately well as chelators.
Gluconate is the most widely used of the organic acid chelators, and has a decades-long record of effectiveness and safety. It is frequently used to correct mineral deficiencies, to treat inflammatory acne, to regulate CD8 T-cells, and for anorexia. Zinc gluconate can also suppress hepatitis symptoms in dogs. There is, however, no reason to think that the gluconate is a highly efficient chelator.
A number of minerals are available as picolinate supplements: boron, chromium, copper, magnesium, manganese, molybdenum, selenium, vanadium, and zinc. Chromium picolinate is widely used to enhance athletic performance, and has been well studied. Vanadyl picolinate shows great promise as a glucose regulator in diabetes. The other picolinates have received very little attention from researchers. It is known that the bioavailability of zinc, copper and magnesium increases significantly when it is combined with picolinic acid in the diet, and that zinc picolinate is superior as a chelate to zinc gluconate and zinc citrate. This scanty information suggests that the picolinates are relatively effective chelators and mineral transporters.
We have a bit more information about the orotates. Magnesium orotate showed good results in studies of athletic performance, both in healthy men and cardiac patients; it improves blood lipid profiles and inhibits arterial plaque formation. Lithium orotate (a freely available nutritional supplement), is at least as good a source of lithium as lithium carbonate (a prescription drug) which is used for treating mental conditions such as manic-depression (bipolar disorder), autism, obsessive-compulsive disorder. Lithium carbonate has also shown benefit in treating the effects of alcoholism. The other orotates have received little research attention except from their developer, Hans Nieper, whose scientific methods left a lot to be desired. The orotates do, however, have a many users and a correspondingly large amount of anecdotal information. For example, calcium orotate is regarded as a good appetite suppressant and cognitive stimulator.
Comparison of chelators
A few researchers have tried to answer the question of which types of chelators produce the highest bioavailabilities of minerals. Theirs were veterinary studies and, unfortunately, they used animals that had first been rendered mineral-deficient by being fed special mineral-deficient diets. This method does not provide information about relative bioavailabilities for the condition we are interested in here, namely: the condition of being a non-mineral-deficient human. We are interested in increasing our intracellular mineral concentrations beyond the levels allowed by ordinary nutrition and by the body’s normal regulatory processes. (See the article Mineral transport.)
The general impression one gets from looking at the published research on this subject is that inorganic salts are adequate mineral sources for correcting dietary mineral deficiencies in healthy people, but that more specialized sources are needed for correcting deficiencies due to disease, or for by-passing the body’s mineral regulators in order to achieve higher-than-normal mineral levels. For these purposes organic salts appear to be better than inorganic salts, and amino-acid chelates appear to be better than the organic salts. Among the organic salts, the picolinates and orotates appear to offer advantages over other available forms.
Future research may paint a rather different picture of the relative values of different mineral transporters than the one painted here. For example, the apparent superiority of the picolinates and orotates is based on indirect evidence, since there is hardly any published research directly comparing the efficacy of these forms with other mineral forms. The orotates remain largely neglected by researchers, and so have the picolinates – with the one exception of Chromium Picolinate. The relative value of different chelators and other transporters may turn out to depend strongly on which mineral one is dealing with, and upon various other factors. For now, our decisions about which mineral supplements to use will have to be guided by the smattering of knowledge available and by our own willingness to experiment with them.
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Heard about CardioPeptase, the proteolytic enzyme sometimes known as serrapeptase or serratiopeptidase? Chances are you haven’t, until now. It’s only been available as a nutritional supplement in the US for the past two years. Yet for over 30 years serrapeptase has been gaining wide acceptance in Europe and Asia as a potent analgesic and anti-inflammatory drug. It’s been used to promote wound healing and surgical recovery. Recent Japanese patents even suggest that oral serrapeptase may help treat or prevent such viral diseases as AIDS and hepatitis B and C. But perhaps its most spectacular application is in reversing cardiovascular disease. In fact, serrapeptase appears so effective in unblocking carotid arteries that one researcher – Dr. Hans Nieper, the late, eminent internist from Hannover, Germany – called it a “miracle” enzyme.
Does this all sound a little too miraculous to be true? Read on. There’s a solid scientific rationale for each of these heath benefits, and they all have to do with the fact that serrapeptase is “proteolytic” (literally, protein-dissolving).
Proteolytic enzymes (also known as proteinases or peptidases) are ubiquitous in nature, being found in animals, plants, bacteria, and fungi. Human beings produce such well known peptidases as trypsin and chymotrypsin to help digest our food, but we also generate countless others to control virtually every regulatory mechanism in our bodies. For example, various peptidases are involved in initiating blood clotting (thrombogenesis) and also in dissolving clots (fibrinolysis); in evoking an immune response and quelling it; and in both promoting and halting inflammation. The mechanism in each case is the ability of the enzyme to cut or cleave a protein target into two or more pieces, usually at very specific cleavage sites. The same mechanism makes it possible for peptidases to inactivate HIV, the AIDS-associated virus, by pruning the viral proteins necessary for infectivity.
The medical use of enzymes as anti-inflammatory agents goes back many years. In the early 1950s it was discovered that intravenous trypsin could unexpectedly relieve the symptoms of many different inflammatory conditions, including rheumatoid arthritis, ulcerative colitis, and atypical viral pneumonia. Subsequently intramuscular enzyme injections were found to be beneficial in counteracting post-surgical swelling (edema), treating thrombophlebitis and lower back strain, and rapidly healing bruises caused by sports injuries.
At that time the mechanism of the anti-inflammatory effect remained obscure. Today it is believed to involve degradation of inflammatory mediators, suppression of edema, activation of fibrinolysis, reduction of immune complexes (antibody-antigen conglomerates), and proteolytic modification of cell-surface adhesion molecules which guide inflammatory cells to their targets. (Such adhesion molecules are known to play an important role in the development of arthritis and other autoimmune diseases.) It’s also thought that the analgesic effect of proteolytic enzymes is due to their cleavage of bradykinin, a messenger molecule involved in pain signalling. However, according to another theory, peptidases such as trypsin may be acting not as anti-inflammatory agents but rather as accelerants of the inflammatory process, thereby shortening its duration. Whatever the mechanism, many studies of proteolytic enzymes over the years have demonstrated their effectiveness in relieving pain and inflammation independently of steroids or nonsteroidal anti-inflammatory drugs (NSAIDs).
Fortunately we don’t need to rely on intramuscular injections any more to enjoy the benefits of proteolytic enzymes. Around 35 years ago researchers showed that enterically-coated enzymes such as trypsin, chymotrypsin or bromelain were orally active. Oral proteolytic enzymes have been used successfully ever since for inflammatory conditions. Recently the intestinal absorption of orally administered serrapeptase has also been demonstrated. To achieve an ideal therapeutic effect, however, it is essential that any enzyme preparation be properly enterically coated so as to release the enzymes in the intestines (where they can be absorbed) and not in the stomach (where they can be digested).
The proteolytic enzymes in common use today derive from bacteria (serrapeptase grown from Serratia marcescens cultures), plants (bromelain from pineapple stem and papain from papaya), and animal sources (trypsin and chymotrypsin from hogs or cattle). They’re all generally useful, but for many applications serrapeptase appears to be the most useful of them all. In one study serrapeptase was compared to trypsin, chymotrypsin, and pronase (another microbial peptidase) in a rat model of scalding, which is known to induce abnormal activation of fibrinolysis. Serrapeptase was far more effective than any other enzyme in repressing fibrinolysis in this model, in agreement with its documented clinical efficacy as an anti-inflammatory agent.
By the way, in case you’ve got a good memory for details, you might have noticed that a few paragraphs back I said the activation of fibrinolysis, not its repression, is one of the likely anti-inflammatory mechanisms of serrapeptase. The truth is that serrapeptase, like other peptidases, can have seemingly contradictory effects at different times under different circumstances. The essential point of the study just cited is that serrapeptase and the other peptidases inhibited abnormal activation of fibrinolysis, and that this was a sign of their anti-inflammatory activity.
In other circumstances serrapeptase is definitely fibrinolytic, i.e., clot-busting, and it is this property that makes it so useful in treating cardiovascular disease. According to Dr. Hans Nieper, only three 5 mg tablets of serrapeptase daily for 12 to 18 months are sufficient to remove fibrous blockages from constricted coronary arteries, as confirmed in many of his patients by ultrasound examination. But that – is still not the whole story – serrapeptase may well offer additional cardiovascular benefits not considered by Nieper. In particular, researchers have recently proposed that inflammation contributes to the development of arterial blockage. In one study, subjects with higher levels of CRP (C-reactive protein, a marker for systemic inflammation) were found to have a greater risk of future heart attack and stroke, independently of other risk factors such as smoking, high blood pressure, or cholesterol levels. Subjects with the highest levels of CRP who also used aspirin, however, showed dramatic decreases in their risk of heart attack, leading the researchers to speculate that the effectiveness of aspirin in preventing heart attack is due as much to its anti-inflammatory activity as to its anticlotting effects.
Serrapeptase, like aspirin, is both anti-inflammatory and anticlotting; unlike aspirin, however, serrapeptase can melt through existing fibrous deposits. Serrapeptase also lacks the serious gastrointestinal side effects associated with chronic use of NSAIDs such as aspirin. This combination of properties makes serrapeptase just about the perfect remedy for warding off cardiovascular disease, better even than the proverbial aspirin a day. It’s beginning to look more and more as though Dr. Nieper was right – serrapeptase is indeed a “miracle” enzyme.
For optimal results in unclogging arteries Nieper suggests combining serrapeptase with other nutritional factors, including bromelain, magnesium orotate, carnitine, and selenium; see the information packet obtainable from the Brewer Library for more details. To avoid possible pulmonary and ileal irritation, Nieper also recommends not exceeding a dose of about three tablets per day for long-term continuous use.
Because serrapeptase is a blood-thinning agent, it’s wise to consult your physician if you’re already taking any form of anticoagulant therapy (or, for that matter, if you suffer from any serious illness). Despite these cautions, however, serrapeptase has an excellent tolerability profile in general. The Japanese company that first developed serrapeptase, recommends up to six 5 mg tablets per day – two tablets three times a day, between meals – for short-term treatment of acute inflammation due to surgery, wound healing, sinusitis, cystitis, bronchial asthma, bronchitis, and breast engorgement in lactating women. (On a personal note, I feel compelled to add an anecdotal observation – my wife finds that six tablets a day are also effective for relieving the pain and edema of PMS-related breast engorgement.)
If you’re already taking proteolytic enzymes such as bromelain or trypsin for sports injuries, arthritis, multiple sclerosis, or any other condition including PMS, try adding or substituting serrapeptase. You just might be amazed with the results. And if you’re not already taking proteolytic enzymes – what are you waiting for? There’s a miracle named serrapeptase waiting to happen for you now.
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This article addresses two biochemical puzzles about the mineral orotates: how they get into cells and what they do once they’re in.
We begin with the fact that the orotate salts are electrically neutral and relatively stable against dissociation, properties that seem to be crucial for the ability of orotates to participate in intracellular mineral uptake and transport. Dissociation is the process that takes place when a salt is dissolved in a solvent such as water and breaks up into its component ions. Table salt dissolved in water, for example, dissociates into sodium and chloride ions. At physiological pH the orotate salts are much more stable than table salt and will not readily dissociate into free orotic acid plus a mineral ion.
Free orotic acid (OA) itself is known to get into cells by simply leaking (diffusing) through cell membranes, rather than by being actively transported. But diffusion is a relatively inefficient process, which limits the amount of OA that can enter a cell. By contrast, uracil – a compound almost identical to OA, only minus the carboxylic acid group – is taken up efficiently by a transporter protein that binds to uracil molecules and drags them into the cell. This transporter appears to be specific for uracil or similar molecules which are uncharged, but not for uracil’s close cousin OA (which is negatively charged at body pH).
Bind the orotic acid with a mineral, however, and you end up with a stable electrically neutral salt. This property is just what is needed for OA along with its bound mineral to be taken up directly by the uracil transporter. At the same time, neutralizing the charge on OA makes the resulting complex more lipophilic or “fat-loving” than free OA; as a result, the stable orotate complex would be expected to diffuse more easily through the lipid membranes of cells. Essentially just such a mechanism was proposed by Nieper for enhancing the diffusion of mineral ions across cell membranes. Either way – via enhanced diffusion or active transport – complexing a mineral with orotate results in increased uptake of both components of the complex by cells.
That’s still not the whole story of orotate, however. Here and there in his papers, Nieper gives tantalizing clues about the role of the “pentose phosphate pathway” or PPP in mediating the effects of his mineral orotates. The PPP is a well-known biochemical cycle which, among other vital functions, is responsible for synthesizing D-ribose 5-phosphate. D-ribose is of course the sugar which gets incorporated into nucleotides (a process known as ribosylation) and ultimately into RNA/DNA. Was Nieper attempting to signal a deep connection between the ribosylation of orotate and its activity as a mineral transporter?
The answer is yes. To see what Dr. Nieper was hinting at, we need some additional background information on OA, also known as vitamin B13.
Although orotic acid isn’t officially considered a vitamin these days, over 40 years ago it was found to have growth-promoting, vitamin-like properties when added to the diets of laboratory animals. Subsequent nutritional studies in humans and animals revealed that OA has a “sparing” effect on vitamin B12, meaning that supplemental OA can partially compensate for B12 deficiency. OA also appears to have a direct effect on folate metabolism.
Many of the vitamin-like effects of OA are undoubtedly due to its role in RNA and DNA synthesis. (B12 and folate are also involved in DNA synthesis, but at a point downstream from where OA comes in.) Our bodies produce OA as an intermediate in the manufacture of the pyrimidine bases uracil, cytosine, and thymine. Together, these pyrimidines constitute half of the bases needed for RNA/DNA, the other half coming from the purine bases adenine and guanine which are synthesized independently of OA.
The enzyme orotate phosphoribosyltransferase (OPRTase), which is found in organisms ranging from yeast to humans, is responsible for catalyzing the first step in the conversion of orotic acid into uridine. It does so by facilitating the attachment of a ribose plus phosphate group to OA. The net result is the formation of a molecule named OMP (orotidine 5′-monophosphate), which in turn is the immediate precursor to UMP (uridine 5′-monophosphate).
Because the enzyme OPRTase requires magnesium ions for its activity, some researchers wondered whether a magnesium complex of orotic acid might be involved in binding orotate to the enzyme. They found that the true substrate for OPRTase is not orotate itself but rather a magnesium orotate complex. The fact that the complex is electrically neutral compared to the negatively charged orotate ion means that the complex is more easily transportable to the active site of the enzyme. These researchers suggested that the magnesium complex helps position orotate within the enzyme in the proper orientation for conversion to OMP. In the process the magnesium ion in the complex gets exchanged with the magnesium ion bound to the active site of the enzyme, the net result being that one magnesium ion is released.
So far, so good. Following up on Nieper’s hint, we see that orotate-and specifically magnesium orotate-can interact with the pentose phosphate pathway (PPP) to generate OMP and ultimately uridine. But Nieper also pointed out that the mineral-transport activity of the orotates does not necessarily have anything to do with the formation of RNA or DNA. To resolve this apparent contradiction, we must seek out an additional metabolic role for orotate independent of RNA/DNA synthesis
In fact, not all the uridine formed from orotic acid does wind up in RNA or DNA. There are other vital roles for orotic acid and uridine in the body-for example, OA gets taken up by red blood cells where it is rapidly converted to UDP-glucose by way of OPRTase and other enzymes. Here UDP is the nucleotide uridine diphosphate. The red blood cells can then act as a storage and distribution pool for delivering glucose and uridine to tissues such as brain, heart, and skeletal muscle. Because UDP-glucose is a precursor for glycogen (a storage form of glucose), the delivery of UDP-glucose to heart muscle and its conversion there to glycogen might account for some of the cardioprotective effects of orotic acid.
Which brings us right back to Dr. Nieper’s work.
Based on the available scientific evidence, it seems clear that magnesium orotate can get channeled directly into OMP synthesis and ultimately into UDP-glucose, which can then resupply a heart under stress with carbohydrates and nucleotides. Thus a mechanism exists for explaining why magnesium orotate works even better than orotic acid for heart conditions. In contrast, some of the mineral orotates such as copper and nickel either inhibit OPRTase or, in the case of calcium orotate, neither activate nor inhibit the enzyme. This suggests that the body preferentially uses magnesium orotate for promoting uridine synthesis. In a sense, complexing OA with magnesium magnifies the “vitamin-like” properties of vitamin B13.
Another effect of magnesium orotate is to inhibit the development of atherosclerosis when administered orally to humans or experimental animals. The animal study in particular tells us that magnesium orotate performs better than orotic acid, which in turn outperforms magnesium chloride, in inhibiting atherosclerotic changes caused by high levels of cholesterol in the diet. In other words, a synergy exists between magnesium and orotic acid such that the complex they form – magnesium orotate – is more potent than either one alone. Dr. Nieper explained this effect by suggesting that when OA in the magnesium orotate complex is coupled with ribose (ribosylated) in the walls of blood vessels, the magnesium ion is liberated during this process and becomes locally available for activating cholesterol-metabolizing enzymes.
The increase in potency of magnesium in going from a chloride salt to an orotate salt is notable and certainly consistent with Nieper’s ideas about orotate as a mineral transporter. But notice that orotic acid also increases in potency in going from free OA to its magnesium complex, an enhancement consistent with the idea that magnesium orotate gets preferentially directed toward uridine synthesis by OPRTase. It is just this combination of properties – enhanced transport of magnesium, itself known for its anti-atherosclerotic and anti-cholesterol effects, and enhanced synthesis of uridine from orotic acid – that makes magnesium orotate so helpful for treating cardiovascular disorders.
By contrast, the very similar compound calcium orotate has none of the effectiveness of magnesium orotate in lowering serum cholesterol, although it does have other characteristics beneficial for treating arterial disease. The difference in activity between magnesium and calcium orotate can best be explained by the specific effects of magnesium in activating cholesterol turnover as well as by the specificity of magnesium orotate-but not calcium orotate-for activating OPRTase.
As the preceding example shows, the various mineral orotates are likely to be targeted to distinct metabolic pathways in specific tissues. Another example is provided by an experiment involving lithium metabolism in the brain. Lithium is well known for its ability to moderate manic-depressive illness. In an experiment to evaluate lithium-induced changes in brain metabolism, rats were injected with a solution of lithium chloride daily for two weeks. One hour after the last lithium treatment all rats received an injection of radiolabeled orotic acid into the cerebral ventricles. At various intervals thereafter RNA was extracted from rat brains, separated into fractions, and analyzed for radioactivity. The results showed that lithium increases RNA turnover markedly in brain (but not in other tissues such as liver). The authors suggested that lithium acts at the membrane level and that the effects on RNA metabolism are due to changes in the transport of radiolabeled orotic acid-an explanation entirely consistent with Nieper’s idea that lithium combines with OA to yield a transportable complex.
In summary, the evidence tends to support Nieper’s criteria for orotate as an electrolyte carrier, namely, (1) a low dissociation constant, (2) an affinity for specific cellular systems or organs, and (3) a metabolic pathway which liberates the transported mineral within the targeted organ or system.