It may well be that the lack of sunshine in the wintertime is the biggest reason we get more colds and flues during that time. It turns out, that sunshine directly charges the immune system – and it has nothing to do with vitamin D!
We suspect that the benefits to heart health of sunlight will outweigh the risk of skin cancer.
And now we may have the missing puzzle piece why…
Sunlight offers surprise benefit — it energizes infection fighting T cells
Georgetown University Medical Center researchers have found that sunlight, through a mechanism separate than vitamin D production, energizes T cells that play a central role in human immunity.
Their findings, published today in Scientific Reports, suggest how our skin – the body’s largest organ – stays alert to the many microbes there.
The study’s senior investigator, Gerard Ahern, PhD, associate professor in the Georgetown’s Department of Pharmacology and Physiology, said:
We all know sunlight provides vitamin D, which is suggested to have an impact on immunity, among other things. But what we found is a completely separate role of sunlight on immunity. Some of the roles attributed to vitamin D on immunity may be due to this new mechanism.
They specifically found that low levels of blue light, found in sun rays, makes T cells move faster — marking the first reported human cell responding to sunlight by speeding its pace.
Ahern says,
T cells, whether they are helper or killer, need to move to do their work, which is to get to the site of an infection and orchestrate a response.
This study shows that sunlight directly activates key immune cells by increasing their movement.
Ahern notes that while production of vitamin D required UV light, which can promote skin cancer and melanoma, blue light from the sun, as well as from special lamps, is safer.
And while the human and T cells they studied in the laboratory were not specifically skin T cells — they were isolated from mouse cell culture and from human blood — the skin has a large share of T cells in humans, he says – about twice the number circulating in our blood.
“We know that blue light can reach the dermis, the second layer of the skin, and that those T cells can move throughout the body,” he said.
The researchers further decoded how blue light makes T cells move more by tracing the molecular pathway activated by the light, Georgetown reported.
What drove the motility response in T cells was synthesis of hydrogen peroxide, which then activated a signaling pathway that increases T cell movement.
Hydrogen peroxide, they reported, is a compound that white blood cells release when they sense an infection in order to kill bacteria and to “call” T cells and other immune cells to mount an immune response.
Amazing, eh!
Ahern concluded [emphasis added]:
We found that sunlight makes hydrogen peroxide in T cells, which makes the cells move. And we know that an immune response also uses hydrogen peroxide to make T cells move to the damage.
This all fits together.
Ahern is eager to continue these findings and figures it might make sense to offer patients blue light therapy to boost their immunity.
What do you think? Have these discoveries made you want to catch some wintry sun?
WASHINGTON, March 9 (Reuters) – About 16 percent of Americans between the ages of 14 and 49 are infected with genital herpes, making it one of the most common sexually transmitted diseases, U.S. health officials said on Tuesday.
Black women had the highest rate of infection at 48 percent and women were nearly twice likely as men to be infected, according to an analysis by the U.S. Centers for Disease Control and Prevention.
About 21 percent of women were infected with genital herpes, compared to only 11.5 percent of men, while 39 percent of blacks were infected compared to about 12 percent for whites, the CDC said.
There is no cure for genital herpes, or herpes simplex virus type 2 (HSV-2), which can cause recurrent and painful genital sores and also increases the likelihood of acquiring and transmitting the AIDS virus. It is related to herpes simplex virus 1, or oral herpes, which causes cold sores.
Several drugs are available to treat herpes symptoms and outbreaks, including acyclovir, which is available generically or under the Zovirax brand name, and valacyclovir, known generically as Valtrex — both made by GlaxoSmithKline PLC (GSK.L). Ganciclovir, sold as Zirgan, is made by privately-held Sirion Therapeutics, Inc.
The CDC estimates that more than 80 percent of people with genital herpes do not know they are infected.
“The message is herpes is quite common. The symptoms can be often very innocuous,” Dr. John Douglas of the CDC said in a teleconference.
“Because herpes is so prevalent it becomes … a really important reason to use condoms on a consistent and correct basis with all of your partners,” Douglas said.
Douglas said the increased rate of infection in blacks is not do to increased risk behavior but likely due to biological factors that make women more susceptible as well as the higher rate of infection within black communities.
The CDC estimates that there are 19 million new sexually transmitted disease infections every year in the United States, costing the health care system about $16 billion annually.
A little over 25 years ago a paper was published in the journal Science showing that BHT, a common food preservative, could inactivate herpes simplex and other lipid-coated viruses in lab dishes. Two years later another paper in the same journal reported similar results, but this time in live animals – dietary BHT could prevent chickens from dying of Newcastle disease. Like herpes simplex, NDV (the virus that causes Newcastle disease) is lipid-enveloped – its nucleic acid core is sheathed in a fatty membrane. Viruses of this type require an intact membrane to be infective. BHT seems to work against such viruses by disrupting their viral membranes.
In the chicken study cited above, the amount of BHT needed to inhibit NDV turned out to be equal to the amount already present in chicken feed as an additive, i.e., 100 to 200 parts per million of total diet. Assuming a comparable result for humans and a total food intake of about 2 kilograms per day, this would mean that 200 to 400 milligrams of BHT ingested daily should be adequate to protect most people from infection by herpes and other lipid-coated viruses.
Inspired by early scientific reports on the antiviral activity of BHT, a number of people suffering from herpes began to experiment on themselves in the late 1970s. As described in several books published a few years later, the BHT experimenters discovered that a daily dose of 250 to 1000 mg resulted in rapid recovery from herpes eruptions with no recurrences.
Studies performed since then have confirmed the activity of BHT against many different human and animal viruses, including such members of the herpes family as CMV (cytomegalovirus), pseudorabies and genital herpes. BHT appears to inhibit infectivity of HIV, the AIDS virus, although contradictory results have also been reported. A protective effect of BHT against the development of influenza infection has been shown. The mechanism involved may have to do with the fact that BHT is a highly potent, membrane-active antioxidant as well as a membrane fluidizer. It’s known that reactive oxygen species (ROS) play a role in the pathogenesis of viral infections – including RNA viruses such as influenza, DNA viruses such as hepatitis B, and retroviruses such as HIV – and it’s been suggested that antioxidants may be useful as therapeutic agents in such infections.
If BHT is so effective against lipid-enveloped viruses, why don’t doctors prescribe it for their patients? The answer is that almost none of the controlled studies on the antiviral properties of BHT have been performed on humans; most of the experiments thus far have been conducted in lab dishes (in vitro) or in animals. A human clinical trial of BHT cannot be performed because the Food and Drug Administration (FDA) has approved BHT for use only as a food preservative, not as a medicine. But that hasn’t stopped some people from using BHT on their own to treat herpes or other viral conditions.
In the past, safety concerns have been sometimes raised about BHT because of its reputed toxicity when given to rats in massive doses – doses much larger than those usually consumed for their antiviral effect. On the other hand, 25 years is long enough for any adverse effects as well as positive benefits to have shown up in humans. Many individuals – including my friend Roger, whom I’ve known since high school – have been supplementing with BHT on a regular basis for years at a time. Roger looks pretty healthy to me these days, but I phoned him anyway to press him for details on his BHT experience.
Roger first began taking BHT in 1984 after reading about it in Pearson and Shaw’s groundbreaking book3. Initially he took about 1 gram per day because he was buying BHT in bulk at the time and larger amounts were easier to measure out than smaller ones. Later he was able to obtain BHT in capsules containing 250 mg per cap, and from that point on he took 250 mg every day for 6 to 7 years. Not surprisingly, during this period he remained completely free of herpes eruptions. More surprising is that he still remains herpes-free to this day, 10 years after his last dose of BHT. Around 3 years ago Roger had a comprehensive physical exam, including blood work. His physician told him that no antibodies to the herpes simplex virus could be found in his system.
Today Roger’s health is generally excellent, with no indication that his years of supplementing with BHT have harmed him in any way. The only adverse effect he ever encountered happened early on, while he was still experimenting with the size of the dose. Roger found that taking 3 grams of BHT each day resulted in dizziness and disorientation, which quickly disappeared when he cut his dose back to 1 gram per day. No adverse effects were seen thereafter.
Of course, a sample of one doesn’t constitute much of a survey. I needed to consult a larger database, so I turned to Steven Fowkes, resident guru at the Cognitive Enhancement Research Institute (CERI) in Menlo Park, California and co-author of Wipe Out Herpes with BHT. Steve Fowkes was unequivocal in his judgment. In the decades since BHT first arrived on the supplement scene, Steve hasn’t heard of any adverse reactions other than two minor ones. First, BHT can cause hives in some people who are sensitive to it. Second, BHT can cause a temporary decrease in blood clotting when people first begin taking it in substantial doses.
Allergic sensitivities to food additives such as dyes and preservatives have been known for some time but the role of these additives in precipitating chronic urticaria (hives) or other symptoms is still a matter of debate. Only a few cases over the years have identified low-level BHT intake as the sole cause of hives, so this reaction is not likely to be very common; however, it may well become more common if provoked by large doses of BHT. Fortunately, the condition tends to clear up after BHT use is halted.
As for the transient blood-thinning effect, Steve cautioned that people who have never taken BHT before should acclimatize themselves by starting out with small doses (less than 250 mg for the first day, if possible) and ramping up gradually over the course of a week; there is a special need for caution among those who are taking anticoagulants at the same time. In no case should the final dose exceed 1 gram per day without medical supervision. BHT’s anticlotting effect will diminish within 2 days in any event, unless extremely high doses (around 5 grams per day or higher) are being taken.
But what about liver toxicity? BHT gets metabolized in the liver, so won’t taking large amounts compromise liver function? Steve’s response was that he has spoken with literally hundreds of people who have successfully treated themselves for herpes with BHT. So long as a dose level of 1 gram per day was not exceeded, no cases of hepatic injury (as determined by pathologically high serum levels of the liver enzymes ALT and AST) have yet been reported by this group.
Unfortunately, some people taking BHT will find that not even 1 gram per day is sufficient to eradicate herpes. Rather than increasing the dose to more than a gram per day, Steve suggests maintaining the BHT level while combining it with other supplements. For example, the combination of BHT with hypericin (from St. John’s Wort) is a synergistic antiviral combination, more effective than BHT alone. To determine an appropriate dose level, hypericin intake should be ramped up gradually from 1 mg per day until an effective dose is reached, usually 10 mg per day or less. Steve also recommended pulsing the hypericin at the effective dose level, i.e., using it for about a week at a time with time off between dosing episodes. Because hypericin can cause photosensitivity of the skin, sun exposure should be limited to half the usual daily amount during and after hypericin intake. One of the nice features of BHT is that it tends to inhibit any oxidative stress induced by hypericin; for this reason, Steve feels that anyone taking hypericin should always take BHT with it.
After talking with Steve Fowkes and reviewing the scientific literature, I’ve concluded that the benefits of taking BHT seem to greatly outweigh the risks. In the process of researching this article I was reminded of a fundamental principle of toxicology first enunciated around 500 years ago by Paracelsus, the great Renaissance physician and alchemist: “All substances are poisons; there is none which is not a poison. The correct dose differentiates a poison from a remedy.” Or in the present case, “the correct dose differentiates a remedy from a food additive.”
BHT and hypericin, two substances available from nutritional supplement distributors, have each shown antiviral activity against herpes viruses and other viruses having lipid envelopes. The antiviral properties of both of these compounds have been investigated scientifically, but the antiviral properties of the combination of the two has so far not been studied except by individuals experimenting on themselves.
Since their mechanisms of antiviral action are different, BHT and hypericin probably act synergistically in the body – that is, their combined effects should be much greater than the effects of either one alone. Each appears to disrupt the lipid envelopes that herpes viruses must have in order to be infective, but BHT does so by dissolving in the envelope and lowering its cohesiveness, whereas hypericin damages the functionality of certain components of the envelope that are required for viral assembly.
Hypericin‘s antiviral effects require that the compound be exposed to light while in the body. Visible light, especially in the orange-to-green wavelengths, appears to be the most effective. UV light also activates hypericin, but carries a higher risk of side effects. Exposure to too much sunlight while using hypericin can cause severe rashes, blistering, and skin damage.
It has been suggested that the antiviral action of hypericin (which involves the generation of free radicals) might be reduced by BHT (which is a quencher of free radicals). Would such a reduction in antiviral activity be large or small compared with the synergistic action of the two compounds? It would probably be quite small, because the compounds would be present in the body in low concentrations. This means that their interactions with each other would be rare events as compared with their interactions with cellular and viral components.
What would a regimen of BHT and hypericin for herpes infections consist of? A reasonable way to start would be to use the two compounds in the same way they are used individually. BHT would be started at 250 mg/day (or less, if possible), and ramped up over a period of a week to no more than 1000 mg/day. Meanwhile, hypericin would be started at 1 mg/day, and ramped up to no more than 10 mg/day. Doses in excess of these amounts should be supervised by a physician. In addition, the parts of the body affected by herpes should be exposed to a bright fluorescent light to activate the hypercin.
Some people have had severe reactions to light when using hypericin. To prevent this, the initial exposure should be only for a few minutes, and then increased gradually over a period of a week or two. In addition, exposure to sunlight should be kept to an absolute minimum.
The reader should bear in mind that these suggestions and precautions are based only on common-sense, and that no actual data is available to support them. As appealing as this combination regimen seems, it does carry unknown risks.
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.
Natural transporters
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.
Artificial transporters
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.
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.
Inorganic salts
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
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.
About chelates
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.)
Organic salts
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.
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.
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.
Have Fruits and Vegetables Become Less Nutritious?
Due to currents levels of soil depletion, genetic modification and pesticides, crops grown decades ago were much richer in vitamins and minerals than the varieties most of us get today. But what’s the nutritional difference between a carrot in 1950s and one today?
Higher antioxidant levels, lower pesticide loads, better farming practices all lead to a more nutritious end product when choosing organic over GMO foods. But the primary culprit in this disturbing nutritional trend is soil depletion: Modern intensive agricultural methods have stripped increasing amounts of nutrients from the soil in which the food we eat grows. Sadly, each successive generation of fast-growing, pest-resistant carrot is truly less good for you than the one before.
A landmark study on the topic by Donald Davis and his team of researchers from the University of Texas (UT) at Austin’s Department of Chemistry and Biochemistry was published in December 2004 in the Journal of the American College of Nutrition. They studied U.S. Department of Agriculture nutritional data from both 1950 and 1999 for 43 different vegetables and fruits, finding “reliable declines” in the amount of protein, calcium, phosphorus, iron, riboflavin (vitamin B2) and vitamin C over the past half century. Davis and his colleagues chalk up this declining nutritional content to the preponderance of agricultural practices designed to improve traits (size, growth rate, pest resistance) other than nutrition.
“Efforts to breed new varieties of crops that provide greater yield, pest resistance and climate adaptability have allowed crops to grow bigger and more rapidly,” reported Davis, “but their ability to manufacture or uptake nutrients has not kept pace with their rapid growth.” There have likely been declines in other nutrients, too, he said, such as magnesium, zinc and vitamins B-6 and E, but they were not studied in 1950 and more research is needed to find out how much less we are getting of these key vitamins and minerals.
The Organic Consumers Association cites several other studies with similar findings: A Kushi Institute analysis of nutrient data from 1975 to 1997 found that average calcium levels in 12 fresh vegetables dropped 27 percent; iron levels 37 percent; vitamin A levels 21 percent, and vitamin C levels 30 percent. A similar study of British nutrient data from 1930 to 1980, published in the British Food Journal,found that in 20 vegetables the average calcium content had declined 19 percent; iron 22 percent; and potassium 14 percent. Yet another study concluded that one would have to eat eight oranges today to derive the same amount of Vitamin A as our grandparents would have gotten from one.
Tomatoes grown by organic methods contain more phenolic compounds than those grown using commercial standards. A study published in the Journal of Agricultural and Food Chemistry analyzed the phenolic profiles of Daniela tomatoes grown either using ‘conventional’ or organic methods, finding that those grown under organic conditions contained significantly higher levels of phenolic compounds than those grown conventionally.
What can be done? The key to healthier produce is healthier soil. Alternating fields between growing seasons to give land time to restore would be one important step. Also, foregoing pesticides and fertilizers in favor of organic growing methods is good for the soil, the produce and its consumers. Those who want to get the most nutritious fruits and vegetables should buy regularly from local organic farmers.
UT’s Davis warns that just because fruits and vegetables aren’t as healthy as they used to be doesn’t mean we should avoid them. “Vegetables are extraordinarily rich in nutrients and beneficial phytochemicals,” he reported. “They are still there, and vegetables and fruits are our best sources for these.”
GMO Foods Are A Source of The Problem
Most nations in the world have no GMO-Free platform to protect their citizens and although this is slowly changing, most nations are far behind places like Ecuador, Peru, Venezuela, Egypt, Russia and others who have GMO-Free or national bans on GMOs. Nations such as The United States, Canada, China, UK, Australia, Mexico, and most of South America, Asia and Africa who have no formal GMO-free platforms so that they continue their unrestricted and widespread use in all foods.
The important thing to note in these deficiencies is that these are exactly the deficiencies in a human being that lead to susceptibility to sickness, disorders and cancer. People who have osteoporosis are low in calcium and magnesium, people who have cancer are low in manganese. The list goes on and on. A stunning report on GMO vs. organic corn posted on Moms Across America clearly showing the nutritional value difference between GMO corn and NON GMO corn.
Non-GMO corn has 6130 ppm of calcium while GMO corn has 14 — non-GMO corn has 437 times more calcium.
Non-GMO corn has 113 ppm of magnesium while GMO corn has 2 — non-GMO corn has about 56 times more magnesium.
Non-GMO corn has 113 ppm of potassium while GMO corn has 7 — non-GMO corn has 16 times more potassium.
Non-GMO corn has 14 ppm of manganese while GMO corn has 2 — non-GMO corn has 7 times more manganese.
Overall, non-GMO corn is 20 times richer in nutrition, energy and protein compared to GMO corn.
Scientists in the United States have developed a flexible microfluidic device that easily sticks to the skin and measures sweat levels to show how the wearer’s body is responding to exercise.
The low-cost device, which can quickly analyses key elements such as lactate, Ph or glucose levels and let the user know if they should stop or change their activity, could also in future help diagnose and monitor disease, the researchers said.
“Sweat is a rich, chemical broth containing a number of important chemical compounds with physiological health information,” said John Rogers, a professor Northwestern University in the United States who led the development of what he called a “lab on the skin”
Reporting results of the trial of the device in the journal Science Translational Medicine, the researchers said one of its attractions is that it allows people to monitor their health on the spot without the need for blood sampling.
The device, a slim, flexible patch measuring less than a couple of centimeters across, has integrated electronics that do not need batteries and can connect wireless to a smartphone.
Rogers explained that during exercise, sweat winds through the tiny microscopic channels of the device and into four compartments. Here, it reacts with chemical reagents to produce color-based readings relating to pH and to concentrations of glucose, chloride and lactate.
The wireless electronics trigger a smartphone app that captures and analyses the image to give the results.
Rogers’ team tested the device on two groups of athletes – one cycling indoors under controlled conditions and the other taking part in a long-distance ride in tough and dry conditions.
The sweat monitoring patch was placed on the athletes’ arms and backs to test its accuracy and durability.
Results showed that with the indoor cyclists, the device’s measurements and readouts were as good as conventional laboratory analyses of the same sweat. In the long-distance cyclists, the device proved robust – it stayed in place, did not leak, and provided good quality readings.
Designed for one-time use of a few hours, the device can also detect a bio-marker for cystic fibrosis, Rogers said, suggesting it could be adapted in various ways to help diagnose disease or monitor health in people with chronic illnesses.
Many teens are afflicted by acne Credit: Telegraph
Spotty teenagers may have the last laugh over their peers with perfect skin after research found that those who suffer from acne are likely to live longer.
Their cells have a built-in protection against ageing which is likely to make them look better in later life, a study has found.
By the time she reaches middle age, the spotty girl who could never find a boyfriend could be attracting envious glances from her grey and wrinkly peers.
“For many years dermatologists have identified that the skin of acne sufferers appears to age more slowly than in those who have not experienced any acne in their lifetime”Dr Simone Ribero, King’s College London
Experts had already noted that signs of ageing such as wrinkles and thinning skin often appear much later in people who have experienced acne.
Now, scientists believe they may have discovered why.
A study of white blood cells taken from individuals affected by spots showed they had longer protective caps on the ends of their chromosomes.
Called telomeres, the caps can be compared with the plastic tips that stop shoe laces becoming frayed.
They help prevent the chromosomes, packages of DNA, deteriorating and fusing with their neighbours during cell division.
Telomeres shrink over time and are closely linked to biological ageing – people with long telomeres age more slowly than people with short ones.
The new research shows that acne sufferers tend to have significantly longer telomeres and may therefore be blessed with the gift of long-lasting youthfulness.
Lead researcher Dr Simone Ribero, from King’s College London, said: “For many years dermatologists have identified that the skin of acne sufferers appears to age more slowly than in those who have not experienced any acne in their lifetime.
“Whilst this has been observed in clinical settings, the cause of this was previously unclear.
“Our findings suggest that the cause could be linked to the length of telomeres which appears to be different in acne sufferers and means their cells may be protected against ageing.
“By looking at skin biopsies, we were able to begin to understand the gene expressions related to this. Further work is required to consider if certain gene pathways may provide a base for useful interventions.”
The study, published in the Journal of Investigative Dermatology, looked at 1,205 female twins, a quarter of whom reported having had acne.
One of the genes involved in telomere length was also found to be associated with acne, suggesting that being spotty did not slow ageing itself but flagged up what was happening in a person’s cells.
Analysis of skin samples from the twins highlighted a gene pathway called p53, which regulates apoptosis, or “programmed cell death” – a kind of cell suicide.
When telomeres become too short, it can trigger a series of events that lead to apoptosis.
The p53 pathway was shown to be less active in the skin of acne sufferers, although this is still under investigation.
Co-author Dr Veronique Bataille, also from King’s College London, said: “Longer telomeres are likely to be one factor explaining the protection against premature skin ageing in individuals who previously suffered from acne.
“Another important pathway, related to the p53 gene, is also relevant when we looked at gene expression in the skin of acne twins compared to twin controls.”
Dandelion has been used medicinally since ancient times for its various health benefits. However, the most powerful benefit to come out of this common weed is something that medical researchers are super excited to have “discovered” – which is its potential to cure cancer!
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This potent root builds up blood and immune system- cures prostate, lung, and other cancers better than chemotherapy. According to Dr. Carolyn Hamm from the Windsor Regional Cancer Centre in Ontario, Canada, dandelion root extract was the only thing that helped with chronic myelomonocytic leukemia. This form of cancer typically affects older adults.
John Di Carlo, who at the time was a 72-year old cancer patient at the hospital, was sent home to live out his final days after all efforts failed to treat his leukemia. He told CBC News that he was advised to drink dandelion root tea as a last ditch effort. Perhaps it should have been the first option offered in his treatment plan, as his cancer went into remission only four months later! His doctors attributed this to the dandelion tea that he drank.
Recent studies have shown that dandelion root extract can work very quickly on cancer cells, as was evidenced in Di Carlo’s case. Within 48 hours of coming into contact with the extract, cancerous cells begin to disintegrate. The body happily replaces these with healthy new cells.
Further studies have concluded that the extract also has anti-cancer benefits for other types of cancer, including breast, colon, prostate, liver, and lung cancer! Dandelion root tea may not taste as pleasant as other teas, but it’s certainly more pleasant than living with the side effects of chemotherapy or radiation treatments.
Traditional cancer therapies harm the immune system by killing all cells, even the healthy ones. Dandelion root has the opposite effect – it actually helps boost your immune system and only targets the unhealthy cells. It’s definitely a win-win situation!
Dr. Hamm warns, however, that dandelion root extract can negatively impact the effects of chemotherapy. It’s always best to consult with your doctor, and let them know any and all supplements or foods that you are consuming on a regular basis.
Screenshot via YouTube
Even if you don’t have cancer, eating the greens or drinking dandelion tea can still give you great health! For example, the roots and stems of dandelion can help fight diabetes. It does this by stimulating the pancreas to produce insulin, which in turn stabilizes the spikes in blood sugar levels.
If you suffer from digestive issues or need to get rid of toxins, dandelion tea may be just what the herbal medicine doctor ordered! The liver aids the digestive system by producing bile, and it also filters the blood of chemicals and other impurities. According to Dr. Axe, the vitamins and minerals found in dandelions can help cleanse the liver and keep it in tip top shape. So by supporting your liver, you are actually creating better health!
Dandelions are also high in antioxidants and vitamin C, which is crucial to helping your body fight off infections, such as the bacteria that cause urinary tract infections. If you suffer from frequent bouts of UTI, drinking dandelion tea on a daily basis may prevent it from happening ever again.
Dandelion greens are bitter, but completely edible – as long as you get it from an area that hasn’t been sprayed with chemicals. The greens are rich in fiber, which is great for intestinal health! High fiber diets have also been shown to reduce the risk of obesity, heart disease, and irritable bowel syndrome.
The greens are also high in vitamin A – just one cup contains 100% of your recommended daily allowance. Vitamin A is critical for maintaining healthy vision, and it can also prevent premature aging of the skin.
Since you probably aren’t likely to eat an entire cup of bitter greens on its own, you can incorporate it into a morning smoothie. Just blend it up with your favorite fruit, which will offset the bitter taste.
Researchers are using algorithms and machine learning to tackle the disease
Microsoft is working towards fighting cancer using computer science such as machine learning and algorithms.
By treating cancer like an information processing system, Microsoft researchers are able to adapt tools typically used to model computational processes to model biological ones.
Ultimately, the company hopes to create molecular computers to program the body to fight cancer cells immediately after detection.
“We are trying to change the way research is done on a daily basis in biology,” said Jasmin Fisher, a senior researcher who works in the programming principles and tools group in the Microsoft’s research lab in Cambridge.
This is combined with a data-driven approach; putting machine learning at the core of Microsoft’s attempts to try to tackle the disease. The company wants to take the biological data that is available and use analysis tools to better understand and treat the disease.
“I think it’s a very natural thing for Microsoft to be looking at because we have tremendous expertise in computer science and what is going on in cancer is a computational problem,” Chris Bishop, director of the Cambridge-based lab, told WIRED.
“It’s not just an analogy, it’s a deep mathematical insight. Biology and computing are disciplines which seem like chalk and cheese but which have very deep connections on the most fundamental level.”
For instance, machine learning and natural language processing are being used to provide a way to sort through the research data available, which can then be given to oncologists to create the most effect and individualized cancer treatment for patients.
At the moment, there is so much data available, it is impossible for a person to go through and understand it all. Machine learning can process the information much faster than humans and make it easier to understand.
Machine learning is also being paired with computer vision to give radiologists a more detailed understanding of how a patient’s tumor is progressing. Researchers are working on a system that could eventually evaluate 3D scans by analyzing pixels to tell the radiologist exactly how much a tumor has grown, shrunk or changed shape since the last scan.
Andrew Phillips, head of the biological computation research group at the Cambridge Lab said researchers benefit from Microsoft’s history as a software innovator.
“We can use methods that we’ve developed for programming computers to program biology, and then unlock even more applications and even better treatments,” he said.
Phillips is working to create a molecular computer that could be put inside a cell to monitor for disease. If the sensor detected a disease, such as cancer, it would activate a response to fight it.
Research such as this would also use traditional computing and re-purpose it into medical or biotechnology applications, so the body could be programmed to fight a disease, in the way we program a computer to do something.
Though the research is still in the early stages, Phillips told The Telegraph it could be technically possible to put in a smart molecular system to fight a disease in this way, in “five to 10 years time”.
Forty-five years after the drug war was declared by President Richard Nixon, the United States leads the world in both recreational drug usage and incarceration rates. Heroin abuse rates continue to soar. Drug-related violence in our nation’s cities and cartel wars in Latin America exact horrific tolls.
And then there is the ever-present bully on the block, prescription drug abuse. More than two million Americans have become hooked on the pharmaceuticals that doctors prescribe to ease their pain. Opioids—both legal and illicit—killed a mind-boggling 28,647 people in 2014.
But not to worry: The Drug Enforcement Administration is on the case. “To avoid an imminent hazard to public safety,” the agency said in a press release, it will be adding kratom, a medicinal herb that has been used safely in Southeast Asia for centuries, to its list of Schedule 1 substances, placing the popular botanical in a class with killers like heroin and cocaine at the end of September.
Why ban the mild-mannered tree leaf? Well, because the DEA claims it’s an opioid with “no currently accepted medical use.” Wrong on both counts.
Pharmacologists label kratom as an alkaloid, not an opioid. True, kratom stimulates certain opioid receptors in the brain. But then, so does drinking a glass of wine, or running a marathon.
Kratom is less habit-forming than classic opioids like heroin and the pharmaceutical oxycodone, and its impact on the brain is weaker and more selective. Nevertheless, the herb’s ability to bind loosely with certain opioid receptors makes it a godsend for addicts who want to kick their habits. Kratom is currently helping wean thousands of Americans off illegal drugs and prescription pain relievers, without creating any dangerous long term dependency.
The powdered leaves are readily available from scores of herb sellers on the Internet. Since the ban was announced in late August, websites and social media have exploded with accounts from people who credit the plant with saving them from lives of addiction and chronic pain.
Take, for example, Virginia native Susan Ash. She was using Suboxone to help cope with severe joint pain resulting from Lyme disease. “My life was ruled by the clock—all I could think was, ‘when do I take my next dose,’” Ash says. Then someone suggested she try kratom to help kick her addiction to the prescription pain killer. “In two weeks time, I went from being a bed-bound invalid to a productive member of society again.
She founded the American Kratom Society in 2014 to help keep this herbal lifeline legal. Ash says that tens of thousands of people use kratom not just to help with chronic pain, but also to alleviate depression and to provide relief from PTSD. She strongly disputes that users like herself are simply exchanging one addictive drug for another.
“I have never had a craving for kratom,” Ash says. “You can’t compare it to even the mildest opiate. It simply won’t get you high.”
What it might do, users say, is slightly tweak your mood. The leaves of the Mitragyna speciosa tree, a biological relative of coffee, have been chewed for centuries in Southeast Asia by farmers to increase their stamina. Kratom is gently euphoric and also relaxing—think coffee without the jitters and sleeplessness. It is hard to take toxic levels of the herb, since larger doses induce nausea and vomiting.
But does it provide medical benefits? Dr. Walter Prozialeck, chair of the Department of Pharmacology at Midwestern University in Downers Grove, Illinois, who conducted a survey of the scant medical literature on kratom, says the herb did indeed help to relieve pain in animal studies.
While no clinical trials have yet been done with humans, addicts in Thailand and Malaysia have used kratom for decades to detox from heroin and alcohol. It was so successful in getting people off opium that Thailand banned kratom in 1943 to stem the loss of the opium taxes that funded the government.
Nobody knows how many are using kratom here in the US. “There are so many testimonials out there [from kratom users] on the Internet that I personally found quite compelling,” Dr. Prozialeck says. “This merits further study.”
But study has proven difficult. Dr. Edward Boyer, director of toxicology at the University of Massachusetts Medical School, says that when he tried to conduct research on kratom, potential partners told him, “we don’t fund drugs of abuse.” Drug companies have shown sporadic interest in isolating the active constituents in kratom since the 1960s, he says, but no pharmaceuticals have yet been developed from them.
Given the current opioid crisis, Boyer hopes researchers will dive deeper into the plant’s pharmacology. “Wouldn’t it be great to have an analgesic that will relieve your pain and not kill you?” Boyer notes that kratom is free from the potentially deadly side effects like respiratory failure that have bedeviled prescription opioids.
However, drug companies have shown little interest in a plant remedy that cannot be patented. While some of kratom’s active ingredients have indeed been patented by researchers who hope one day to market them to pharmaceutical firms, Boyer said that these compounds have failed to exhibit as powerful pain-killing effects as the whole plant. “There is something in there that we don’t yet understand,” he added.
And if the DEA’s ban goes into effect, we may never understand kratom’s remarkable potential. That’s because the federal action would have a chilling effect on research, according to Boyer.
The DEA claims that kratom is addictive. Since you can get hooked on most anything— even coffee or chocolate, as Dr. Boyer pointed out, this claim is both relatively meaningless and also hard to dispute. Users report that withdrawal symptoms from kratom are comparable to giving up coffee—a few days of irritability, perhaps a headache.
In issuing its scheduling notice, the DEA said that the Centers for Disease Control received 660 complaints about kratom (including reports of constipation and vomiting) between 2010 to 2015, out of 3 million calls annually reporting adverse reactions to assorted other foods and drugs. To put this number in perspective, the National Poison Data System registers more than 3,700 calls about caffeine annually, every year leading to multiple overdoses that result in death.
“This hardly constitutes a public health emergency,” says Susan Ash. “They definitely get more calls about energy drinks.”
In banning kratom, the DEA dispensed with the usual public comment period. Advocates, however, refuse to be silenced. They plan to challenge the DEA’s action in court and are marching on the White House on September 13. A petition urging President Barack Obama to reverse the ban has surpassed the 100,000 signature mark which, by law, requires a personal response from the president.
“There is a cheap plant out there that’s helping people getting off opioids,” Ash says, “and now so many are going to be forced back into active addiction, or made a prey to black market drug dealers.”
What if, instead of turning tens of thousands of law-abiding Americans into either addicts or felons, the DEA listened to those who have used kratom successfully to kick their addictions and manage chronic pain? Instead of banning the herb, why not draft some sensible regulation to establish dosage and labelling requirements and to protect consumers from adulterated product?
And while they are at it, America’s drug agency should sponsor some long overdue scientific research into a substance that may be the best thing going to combat our runaway epidemic of opioid addiction.
A little over 25 years ago a paper was published in the journal Science showing that 
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