Thyroid supplements

People typically seek thyroid support nutrients as a way to enhance their energy levels, enable proper control of their body temperature, and support a strong metabolic rate.  We take these nutrients, both individually and in formulas, in order to assure adequate levels to support optimal thyroid function, since a deficiency or insufficiency of key nutrients could reduce the operational efficiency of the thyroid gland.   Proper thyroid function supports a lean body composition and helps prevent fatigue.  Under the control of complex feedback and signals from the hypothalamic-pituitary-thyroid axis, the thyroid gland regulates body temperature and metabolism rates, playing an important role in weight management and energy states.  By the same token, if any of the important nutrients are not available to the thyroid in sufficient amounts, metabolic rates and energy levels could suffer. ¹

Natural thyroid support supplements work primarily by providing precursors of thyroid hormones, along with various cofactors, in order to encourage proper thyroid function.  In some cases, the lack of adequate nutritional resources prevent the thyroid gland from maintaining optimal efficiencies, and if the gland can’t maintain healthy levels of its important hormones, then it can’t adequately support the body’s metabolism.  Unlike medical treatments, nutritional approaches focus on providing what the body needs in order to assure that the thyroid has its particular needs met and can function optimally. 

The key nutrients for thyroid function are the mineral Iodine and the natural amino acid L-Tyrosine. 

Humans require iodine for cellular metabolism and for normal thyroid function; specifically for the production of thyroid hormones.  Thyroid hormones regulate many important biochemical reactions, including protein synthesis and enzymatic activity, and are critical determinants of metabolic activity.  Iodine is a nutrient that can sometimes be obtained from the soil, but many soils are deficient.  Areas that are mountainous, very rainy, or prone to floods/erosion tend to have soils that are low in iodine, increasing the risk that foods grown in those areas will be iodine-deficient.  Table salt is commonly iodized, but those using non-iodized salt or on low-sodium diets can’t rely on that source.  Multivitamin formulas, thyroid support formulas, kelp and some other seaweeds, and some multimineral formulas provide supplemental iodine.  The U.S. Recommended Dietary Allowance (RDA) is 150 mcg (micrograms) daily for adults ages 18 and older, 220 mcg daily for pregnant women, and 290 mcg daily for lactating women. The Tolerable Upper Intake Levels (UL) for adults ages 18 and older is 1,100 micrograms daily. ^{2-3 ]}

The common sources of iodine in dietary supplements include Potassium Iodide, Kelp, and other seaweeds.  While kelp and some seaweeds are fine for getting the relatively low RDA level of iodine intake, those seeking much higher levels are usually advised to consider Potassium Iodide.  This is because seaweeds typically contain less than 1% iodine, along with a lot of other metals and minerals - including some that we may want to avoid getting too much of - so consuming high doses of seaweeds on a daily basis may not be our safest option.  And iodine is a mineral nutrient that needs to be replenished daily.

L-Tyrosine is an amino acid that is important to the structure of most proteins in the body. It is also the precursor of a number of neurotransmitters and hormones, including the major catecholamines dopamine, norepinephrine, and epinephrine (adrenaline), which are stress hormones made by the adrenal glands.  In addition to these functions, tyrosine also helps produce melanin (the pigment responsible for hair and skin color) and helps in the function of the adrenal, thyroid, and pituitary glands.  Because of these varied responsibilities and the ability of various stresses and dietary deficiencies to reduce tyrosine levels, people sometimes supplement tyrosine (as natural L-Tyrosine) in order to support proper thyroid function. ^4-5   

How do Iodine and L-Tyrosine affect thyroid function?  The thyroid gland’s epithelial cells prepare large quantities of tyrosine into a glycoprotein “scaffold” that is the structural backbone used to form the thyroid hormones thyroxine (T4) and triiodothyronine (T3).  The scaffold and iodine are both secreted into the lumen of the thyroid gland, where an enzyme facilitates the hormone synthesis.  Other enzymes then separate the hormones from the scaffolding in steps, liberating them into their circulating forms.  A few tyrosines are incorporated into these hormones, but most are left in the scaffolding structure’s remains that will be recycled by the body. 

Selenium is an essential mineral nutrient that is necessary for normal thyroid hormone metabolism.  Selenium-containing enzymes control the synthesis and degradation of the biologically active thyroid hormone, T3.  Selenium deficiency may worsen the effects of iodine deficiency on thyroid function, and adequate selenium nutritional status may help protect against some of the neurological effects of iodine deficiency.   Additionally, selenium-based antioxidant enzymes protect the thyroid gland from peroxides produced during the synthesis of these hormones. ^{2, 3, 6}

Zinc, another essential mineral responsible for hundreds of critical chemical reactions in the healthy human, is also important for maintaining normal thyroid homeostasis. Its complex roles include effects on both the synthesis and mode of action of the hormones.  Thyroid hormone binding transcription factors, which are essential for modulating gene expression, contain zinc bound to cysteine-related compounds.   In some studies, low zinc status was associated with decreased thyroid hormone levels.  ³

Copper is believed to have a role in thyroid hormone function, perhaps related to selenium status. ³

Guggul (Commiphora mukul) is an Indian Ayurvedic herb that contains the active compound Guggulsterone, which has been shown to stimulate thyroid activity. ^7-8

 
These ingredients, both singly and as thyroid support formulas, are in demand by consumers wanting to assure adequate thyroid function in times of dietary insufficiencies and various stresses.  Of course, these nutrients and their many functions in the body have a host of potential benefits to those supplementing with them if they may not get adequate amounts from their diet for their individual requirements. 

 

REFERENCES

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1.  Zoeller RT, Tan SW, Tyl RW. General background on the hypothalamic-pituitary-thyroid (HPT) axis. Crit Rev Toxicol. 2007 Jan-Feb;37(1-2):11-53. Review. PubMed PMID: 17364704.
2. http://ods.od.nih.gov/factsheets/Iodine-HealthProfessional/
3. Arthur JR, Beckett GJ. Thyroid function. Br Med Bull. 1999;55(3):658-68. Review. PubMed PMID: 10746354.
4. http://www.umm.edu/altmed/articles/tyrosine-000329.htm
5. http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/thyroid/synthesis.html
6. http://ods.od.nih.gov/factsheets/selenium/
7. http://www.drugs.com/npp/guggul.html
8. http://www.peoplespharmacy.com/2005/10/18/guggul/

How Nutrition Affects Swine Flu (Influenza) and Immunity

Why are the Public Health authorities silent on the role of nutrition to protect us during an official national health emergency? Do they not know, or simply not care? Is either answer acceptable to citizens concerned about their health and wanting to get practical/real/fair/impartial information that we can utilize to help protect our families? Here's what the experts are not telling us:

• Did you know that if you had the seasonal flu vaccine last year it may make you more vulnerable to the swine flu this year? Vaccines create antibodies that actually make you more susceptible to other organisms, like viruses and bacteria. (Four Canadian studies reported by CBC News, 9/23/09)
• Did you know that side effects of vaccines can be minimized if there are adequate levels of vitamin D in the person? (Epidemic influenza and vitamin D. Epidemiol Infect. 2006 Dec;134(6):1129-40. Review.)
• Did you know that a lack of vitamin D makes people far more likely to have respiratory infections? (On the epidemiology of influenza. Virol J. 2008 Feb 25;5:29. Review.) Did you know that the virus itself can become less aggressive and less prone to mutating into more dangerous forms if a person has adequate levels of nutrients, especially antioxidants? (Host nutritional status: the neglected virulence factor. Trends Microbiol. 2004 Sep;12(9):417-23. Review.)
• Did you know that antioxidants, like selenium, not only reduce our vulnerability to getting influenza but also reduce the chances that it will progress into pneumonia! (Host nutritional status: the neglected virulence factor. Trends Microbiol. 2004 Sep;12(9):417-23. Review.)

Selenium Safety

Selenium Safety By Neil E. Levin, CCN, DANLA 9/21/07 My comments refer to “Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group” 1 Giving high doses of a single antioxidant is contrary to the realities biology and nutrition. It is unfortunate that synergistic nutrients are tested individually, like drugs. This is a pharmaceutical practice, not human nutrition, and also shouldn’t imply that comprehensive mixtures of nutrients (like a multivitamin) would have the same effects. Additionally, giving these doses to sick patient populations typically results in the authors’ cautions that their results are not applicable to the general population. Still, this disclaimer is routinely ignored in the significant portion of the media that tends to sensationalize the results in headlines or brief televised “health segments”. Antioxidants are synergistic and simply don’t work in isolation. In fact, high doses of single antioxidants have been shown to create imbalances, in vivo, and may even backfire. I consider these cases to be a fault of the study design and a lack of understanding of the scientific field, not a defect of the nutrient being studied. This report was primarily a study of patients with skin cancers, with a increase in self-reported Type 2 diabetes found during a “secondary analysis”. This means that strict elimination of various factors and strict screening of patients was not completed in relation to this unexpected outcome, and that researchers relied primarily on patients’ anecdoctal reports of being diagnosed with diabetes during the trial. This raises issues of undiagnosed cases of diabetes at the start of or during the trial, since even a few missed diagnoses could have (admittedly) reduced or eliminated the significance of the results. Admittedly, “detailed information on unmeasured risk factors at baseline, such as family history of diabetes, body fat distribution, and physical activity, are lacking.” This expands the variables far beyond those accounted for in the study design, which was really looking at cancer recurrences. (More on that later.) Other concerns with this report: • Only Caucasians were included in the patient population; almost all participants in the NPC trial were non-Hispanic white persons. Three-quarters of participants were men. • Patient compliance was also self-reported, limiting validity of the data. • Selenium is not an antioxidant commonly associated with glucose metabolism, so its selection is a bit odd, though in some past studies the mineral has given some indications that it may be useful. However, its close association with vitamin E, and the lack of data on coinciding use of that and other antioxidants, raises more questions than answers. Selenium was used in a study primarily looking at its effect on cancer, with good reason based on past science, and with self-reported diabetes only noticed as varying between the groups incidentally. • The “risk for type 2 diabetes did not differ between treatment groups within the top tertile of BMI” (Body Mass Index, indicating the most overweight people). This strongly indicates another possible variable and alternative explanation, reducing the validity of the implication that selenium alone was the cause of the increased diabetes self-reports. • A well known, name-brand selenium supplement was changed for a different one late in the study, without explanation. • High-selenium yeast products may not work the same as selenomethionine, the most popular type of selenium supplement currently sold. And yeast itself is considered to be a good dietary source of selenium and other nutrients, yet yeast was the placebo. • The population was consuming more than the Daily Value of selenium in their diet, so this was not a particularly selenium-deficient group before supplementation. And since they had all had previously diagnosed skin cancer, it appears that significant other factors, especially antioxidant synergies, were lacking in this patient group. The researchers admit that, “we cannot rule out the role of chance in our findings.” In other words, they admit that their report doesn’t really prove anything. In fact, in the original trial, the focus was on selenium and cancer. What were those results? Selenium alone so successfully reduced cancer incidences and cancer mortality that the study was halted early because a lack of selenium was so clearly associated with higher incidences and deaths from cancer. “Primarily because of the apparent reductions in total cancer mortality and total cancer incidence in the selenium group, the blinded phase of the trial was stopped early. No cases of selenium toxicity occurred. CONCLUSIONS: Selenium treatment did not protect against development of basal or squamous cell carcinomas of the skin. However, results from secondary end-point analyses support the hypothesis that supplemental selenium may reduce the incidence of, and mortality from, carcinomas of several sites.” 2, 12 Regarding the editorial about selenium and diabetes published in the same edition of the journal Annals of Internal Medicine, negative comments were made about the general safety of antioxidant supplements. 3 I dispute that “randomized, controlled clinical trials have shown that ß-carotene and vitamin E supplements, which were widely believed to be safe, increase mortality and morbidity”. The choices, increasing variables, and manipulation by statistical models in meta-analyses are often questionable. In this report, prediabetic symptoms were not even considered as a variable. Buijsse noted that high carotenoid intake, confirmed by measures of blood levels, was associated with lower mortality rates among the elderly over a ten-year period, countering the claim that ß-carotene dangers are proven. 5 The Miller meta-analysis 9, cited as proof of vitamin E’s dangers, was heavily criticized in published responses, and its conclusions were NOT replicated when the same data was re-analyzed (Hathcock) 7. It should therefore not be cited as proof of the vitamin’s danger. Another meta-analysis cited reported that antioxidant vitamins may increase death rates. But the authors did not determine a dose-dependent or cause-and-effect relationship between antioxidants and deaths (from all causes) of study participants. The researchers pooled 68 published trials, excluding 405 published studies with no deaths reported. Too wide a range of potencies (Vitamin A 1333 IU - 200,000 IU, vitamin E 10 IU to 1000 IU), and durations (28 days to 12 years) were lumped together. 4 The editorial statement, “No dietary supplement, including selenium, has proven useful so far for the prevention of cardiovascular disease or cancer in the general U.S. population,” is questionable. The Alpha-Tocopherol, Beta- Carotene Cancer Prevention (ATBC) Study published by the National Cancer Institute demonstrated a 32% reduction in prostate cancer incidence in response to daily alpha-tocopherol supplementation. 8, 10 The Women’s Health Study (JAMA) reported a significant 24% reduction in cardiovascular death with supplemental vitamin E. 11 The NIH reports, “Taking a daily supplement containing 200 mcg of selenium … significantly reduced the occurrence and death from total cancers. The incidence of prostate cancer, colorectal cancer, and lung cancer was notably lower in the group given selenium supplements.” 13 Yet the Annals editorial suggests lowering consumption below the Daily Value (70 mcg) used in multivitamins, far below the current official upper limit of 400 mcg. 13 On the contrary, the Lewin Group reports that the use of antioxidants could save the vision and independence of many senior citizens, saving billions of dollars in healthcare costs. 6 REFERENCES: 1. Stranges S, et al. Effects of long-term selenium supplementation on the incidence of type 2 diabetes: a randomized trial. Ann Intern Med. 2007 Aug 21;147(4):217-23. Epub 2007 Jul 9. Summary for patients in: Ann Intern Med. 2007 Aug 21;147(4):I14. PMID: 17620655 [PubMed - indexed for MEDLINE] 2. Clark LC, Combs GF Jr, Turnbull BW, Slate EH, Chalker DK, Chow J, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group. JAMA. 1996;276:1957-63. 3. J. Bleys, A. Navas-Acien, and E. Guallar. Selenium and Diabetes: More Bad News for Supplements. Ann Intern Med, August 21, 2007; 147(4): 271 - 272. 4. Bjelakovic G, et.al. Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention: Systematic Review and Meta-analysis. JAMA 2007. 297(8):842-857 5. Buijsse B, et al. Plasma carotene and alpha-tocopherol in relation to 10-y all-cause and cause-specific mortality in European elderly: The Survey in Europe on Nutrition and the Elderly, a Concerted Action (SENECA). Am J Clin Nutr 2005;82:879–886. 6. DaVanzo JE, et al. An Evidence-Based Study of the Role of Dietary Supplements in Helping Seniors Maintain their Independence. The Lewin Group Inc. January 20, 2006 7. Hathcock JN, et al. Vitamins E and C are safe across a broad range of intakes. Am J Clin Nutr. 2005 Apr;81(4):736-45. Review. PMID: 15817846 8. Weinstein SJ, et al. Serum alpha -Tocopherol and gamma-Tocopherol in Relation to Prostate Cancer Risk in a Prospective Study. J. Natl. Cancer Inst. 2005 97: 396-399; doi:10.1093/jnci/dji045 9. Edgar R. Miller, III, MD, PhD; et al. High-dose vitamin E supplementation may increase all-cause mortality, a dose response meta-analysis of randomized trials. Annals of Internal Medicine. 4 January 2005 | Volume 142 Issue 1 10. Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study Group. The effect of vitamin E and beta-carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029 –35. 11. Lee IM, et al. Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women's Health Study: a randomized controlled trial. JAMA. 2005 Jul 6;294(1):56-65. PMID: 15998891 12. Combs GF Jr, Clark LC, Turnbull BW. Reduction of cancer risk with an oral supplement of selenium. Biomed Environ Sci. 1997 Sep;10(2-3):227-34. PMID: 9315315 13. Dietary Supplement Fact Sheet: Selenium. Office of Dietary Supplements • NIH Clinical Center • National Institutes of Health. http://ods.od.nih.gov/factsheets/selenium.asp

Selenium and Antioxidant Safety

My letter criticizing their editorial in Annals of Internal Medicine was accepted and published online by that journal: http://www.annals.org/cgi/eletters/0000605-200708210-00177v1#21702 It is unfortunate that synergistic nutrients are tested individually, like drugs. This is a pharmaceutical practice, not human nutrition, and shouldn’t imply that comprehensive mixtures of nutrients (like a multivitamin) would have the same effects. I dispute that “randomized, controlled clinical trials have shown that ß-carotene and vitamin E supplements, which were widely believed to be safe, increase mortality and morbidity”. The choices, increasing variables, and manipulation by statistical models in meta-analyses are often questionable. In this report, prediabetic symptoms were not even considered as a variable. Buijsse noted that high carotenoid intake, confirmed by measures of blood levels, was associated with lower mortality rates among the elderly over a ten-year period, countering the claim that ß-carotene dangers are proven. The Miller meta-analysis, cited as proof of vitamin E’s dangers, was heavily criticized in published responses, and its conclusions were NOT replicated when the same data was re-analyzed (Hathcock). It should therefore not be cited as proof of the vitamin’s danger. Another meta-analysis cited (Bjelakovic) reported that antioxidant vitamins may increase death rates. But the authors did not determine a dose-dependent or cause-and-effect relationship between antioxidants and deaths (from all causes) of study participants. The researchers pooled 68 published trials, excluding 405 published studies with no deaths reported. Too wide a range of potencies (Vitamin A 1333 IU - 200,000 IU, vitamin E 10 IU to 1000 IU), and durations (28 days to 12 years) were lumped together. The statement, “No dietary supplement, including selenium, has proven useful so far for the prevention of cardiovascular disease or cancer in the general U.S. population,” is questionable. The Alpha-Tocopherol, Beta- Carotene Cancer Prevention (ATBC) Study published by the National Cancer Institute demonstrated a 32% reduction in prostate cancer incidence in response to daily alpha-tocopherol supplementation. The Women’s Health Study (JAMA) reported a significant 24% reduction in cardiovascular death with supplemental vitamin E. The NIH reports, “Taking a daily supplement containing 200 μg of selenium … significantly reduced the occurrence and death from total cancers. The incidence of prostate cancer, colorectal cancer, and lung cancer was notably lower in the group given selenium supplements.” Yet you suggest lowering consumption below the Daily Value (70 μg) used in multivitamins and far below the current upper limit. On the contrary, the Lewin Group reports that the use of antioxidants could save the vision and independence of many senior citizens, saving billions of dollars in healthcare costs. REFERENCES: Bjelakovic G, et.al. Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention: Systematic Review and Meta-analysis. JAMA 2007. 297(8):842-857 Buijsse B, et al. Plasma carotene and alpha-tocopherol in relation to 10-y all-cause and cause-specific mortality in European elderly: The Survey in Europe on Nutrition and the Elderly, a Concerted Action (SENECA). Am J Clin Nutr 2005;82:879–886. DaVanzo JE, et al. An Evidence-Based Study of the Role of Dietary Supplements in Helping Seniors Maintain their Independence. The Lewin Group Inc. January 20, 2006 Hathcock JN, et al. Vitamins E and C are safe across a broad range of intakes. Am J Clin Nutr. 2005 Apr;81(4):736-45. Review. PMID: 15817846 Weinstein SJ, et al. Serum α -Tocopherol and γ-Tocopherol in Relation to Prostate Cancer Risk in a Prospective Study. J. Natl. Cancer Inst. 2005 97: 396-399; doi:10.1093/jnci/dji045

Antioxidant Confusion

Antioxidant Confusion By Neil E. Levin, CCN, DANLA Board certified clinical nutritionist with diplomate in advanced nutritional laboratory assessment March 2, 2007 A meta-analysis published in the medical journal JAMA this week reported that antioxidant vitamins do not extend life and may even increase death rates slightly. 1 These conclusions make no sense, based on the scientific record. A meta-analysis relies on a statistical model of existing science, and this model has severe limitations. Even the authors admit some of the basic problems inherent in this type of analysis. More importantly, the authors could not find a dose-dependent or cause-and-effect relationship between antioxidants and deaths (from all causes) of study participants. In other words, they couldn’t show that antioxidants actually caused any deaths or that there was risk at a particular dosage. Yet this questionable speculation received widespread publicity from the sensation-hungry media during “Sweeps Month”, dutifully spreading the lie that antioxidants are now worthless and dangerous. The researchers pooled 68 previously published trials but arbitrarily excluded all published studies that had no deaths reported from any cause. Indeed, 405 otherwise eligible studies were excluded solely for this reason, which if included would likely have dramatically changed the results and conclusion. The researchers did not disclose why they decided to exclude these. This is equivalent to playing a card game after removing all but 7 cards from the deck. (That wouldn’t be a fair game, would it?) They largely ignored the original outcome measures of the studies, many of which had shown positive results for antioxidants, to look only for deaths from any cause in a tiny segment of all published research. This arbitrary decision echoes a frequently cited complaint by scientists commenting to the journal Annals of Internal Medicine when the infamous Miller meta-analysis of vitamin E was released a few years ago, which led to a dramatic slowdown of vitamin E sales. 2 It is interesting that the Miller study’s negative conclusions about vitamin E safety have since been thoroughly debunked by a more rigorous analysis published in the American Journal of Clinical Nutrition by leading antioxidant experts. 3 It is even more interesting that the flawed Miller review was cited as a reference by the JAMA authors but the second, more thorough analysis of the same data by real nutrition experts was not. The lesson learned is that a flawed meta-analysis of nutrients by statisticians and physicians may not hold up to a more competent review done by actual experts in the field of nutrient interactions, though the initial report may have scared people and changed their behavior. Critical comments and corrections typically go ignored, uncited and unreported, in contrast with the sensational initial report. 4 I question both the selection of studies reviewed and the references cited in this meta-analysis. Obviously, excluding six times as many potentially eligible studies as were actually chosen solely because of a requirement that someone in the study population had to die unfairly magnifies negative results by dramatically reducing the pool of studies with potentially positive results and healthier populations. This negative shift is a result of limiting the combined patient population to those studies with at least one dying patient. This population shifts to those individuals who are more likely to be deficient in a variety of antioxidant substances and who are unlikely to respond to limited amounts of one or few supplemental antioxidants. The lack of additional supporting antioxidants may even sometimes increase the oxidative stress on the body. A review of antioxidant science noted, “These negative results…should not be taken as evidence that the free radical theory of aging is flawed. In fact, they prove merely that a complex organism like a human or rodent is unlikely to respond predictably to crude manipulations such as supplementation with one or a small number of compounds.” 1, 5, 6 This mirrors the JAMA authors’ admissions that “antioxidant supplements may show interdependency and may have effects only if given in combination,” and that their findings “should not be translated to potential effects of fruits or vegetables,” which are sources of numerous and varied antioxidant substances. 1 Previous studies have shown the folly of such a protocol. Some years ago an antioxidant study in Finland was halted early because of a widely reported increase in cancer rates among male smokers taking beta-carotene. 7 Headlines associated this supplement with cancer risk. Despite objections that the study was flawed, beta-carotene use dropped. A later analysis published in July 2004 took another look at that same Finnish smokers' study data, but now taking into account total antioxidant intake, which (should have) cleared away the scientific controversy. 8 A composite antioxidant index was generated for each of the 27,000 men over 14 years. The calculated amounts of carotenoids, flavonoids, Vitamin E, selenium and Vitamin C were compared to actual lung cancer rates, with a clear result: an increased intake of a combination of antioxidants lowered lung cancer risk in male smokers. Another large study has noted that high carotenoid intake, as confirmed by measures of blood levels, was associated with lower mortality rates among the elderly over a ten year period. 9 The dietary level of antioxidants is an independent predictor of plasma beta-carotene, especially in moderate alcohol drinkers. A more recent study reports, “This may explain, at least in part, the inverse relationship observed between plasma beta-carotene and risk of chronic diseases associated to high levels of oxidative stress (i.e., diabetes and CVD), as well as the failure of beta-carotene supplements alone in reducing such risk.” 10 In other words, we shouldn’t expect one or two supplemented antioxidants to compensate for a deficiency of total antioxidants in the diet. In fact, many of the protocols for supplementation in the included studies may have actually been of too low potency to achieve noticeable health benefits by remedying latent nutrient deficiencies in fragile patient populations. In other words: many of the interventions were too little, too late. Don’t blame the vitamins. The JAMA report admits that the study populations, the variety of antioxidants used, their potencies and the protocols for taking them were extremely variable, complicating their data with many uncompensated variables. Yet the authors actually claim that, “This increases the trustworthiness of our findings.” I don’t think so! One trial included gave only a single serving of antioxidants and then monitored participants for 3 months. Others used doses of as little as 10 IU of vitamin E (a low amount that is below the Daily Value) and 20 mcg of selenium 1 (an amount far below the 70 mcg DV and not anywhere near the 200+ mcg/day associated with lower cancer rates). 11, 12 I am not alone in these criticisms. Alexander Schauss, PhD, FACN has written, “The range of doses in the different trials they selected for the meta-analysis is dramatic. For example, vitamin A ranged from 1333 IU to 200,000 IU, and vitamin E from 10 IU to 1000 IU. The duration of the studies range from 28 days to 12 years. Nevertheless they were all lumped together.” An Associated Press article quoted other experts criticizing this meta-analysis: ‘Meir Stampfer, professor of nutrition and epidemiology at the Harvard School of Public Health, said the new analysis hasn't discouraged him from taking his vitamins. Stampfer said the studies were too diverse to pool together because they looked at various combinations and doses of antioxidants tested in different groups of people. The trials ranged from a three-month study of 109 elderly nursing home residents to a 12-year study of 22,071 male doctors. "This study does not advance our understanding, and could easily lead to misinterpretation of the data," said Stampfer, who was not connected to the new report.’ The AP report also quoted Donald Berry, chairman of the department of biostatistics at the University of Texas’ M.D. Anderson Cancer Center, stating that this expert also disagreed with the researchers' finding of an increased risk of dying. "There are so many choices you can make when you're doing these analyses," he said. A study of approximately 90,000 nurses suggested that the incidence of heart disease was 30% to 40% lower among nurses with the highest intake of vitamin E from diet and supplements. Researchers found that the apparent benefit was mainly associated with intake of vitamin E from dietary supplements. High vitamin E intake from food was not associated with significant cardiac risk reduction. 13 Levels of Vitamin E above 100 IU daily are associated with decreased risk of coronary heart disease and certain types of cancer, as well as enhancement of immune function. These increased vitamin E intakes are considerably above levels obtainable from diet alone. 14, 15, 16 In a report on the Women’s Health Study published in JAMA, subjects supplementing with vitamin E were reported to have a significant 24% reduction in cardiovascular deaths. 17 Have these previously published benefits of antioxidants miraculously vanished simply because some doctors manipulated a statistical model to elicit unreliable data with no solid basis? Many of the studies included were of patients with specific, serious medical conditions, including one of elderly nursing home patients measuring incidences of bacterial infections (contrasting with a 2004 study published in JAMA noted that, “we observed a protective effect of vitamin E supplementation on upper respiratory tract infections, particularly the common cold, that merits further investigation.” 18), patients with tumors removed from their colon/rectum (antioxidants are associated with apoptosis, a desirable change that leads to death of cancer cells 19, 20), patients with age-related macular degeneration (a condition associated with a deficiency of various antioxidants 21-24), patients with coronary heart disease (a condition related to oxidative damage 14-16), dialysis patients with a history of cardiovascular disease (a condition related to oxidative damage that is reduced by supplemental vitamin E 17), cataract patients (another condition related to oxidative damage 25), male cigarette smokers/present and former cigarette smokers/asbestos workers (all related to low levels of total antioxidants and high toxic load), as well as patients with alcoholic hepatitis, cirrhosis, lupus, heart failure, ALS, etc. This meta-analysis will not stand the test of time because of its many variables, flaws and the arbitrary structuring of its statistical model. When better studies exist, often supported by blood assays, that show higher serum antioxidant levels reduce actual death rates in large populations, then no arbitrary statistical model should be able to negate that robust science with a merely theoretical danger based on such preliminary, questionable criteria. All studies cited here were published in peer-reviewed scientific journals, but that does not make them all of equal quality. Remember my story of the meta-analysis on vitamin E that was refuted by a better meta-analysis, yet both were peer-reviewed? A meta-analysis has more validity if fewer variables are included and if the selection of studies included is not biased by a presumed conclusion. Were hundreds of studies without dying participants ineligible for this particular meta-analysis review simply because of a selection bias, with an intent to demonstrate the dangers of supplementation? These scientists should know better. I see their report as an ill-disguised partisan attack by medical special interests on dietary supplements, a smokescreen for those that don’t look at the quality and quantity of well-designed studies that do show the benefits of vitamins to protect health and prevent deaths. The Lewin Group has presented evidence that the use of antioxidants could save the vision and independence of many senior citizens, while saving the public billions of dollars in healthcare costs. 26 The Institute of Medicine, part of the National Institutes of Health, after reviewing hundreds of well-designed studies, has set safe upper limits for several antioxidants at levels far above the Daily Values. 27 Antioxidants are safe, and proven so in better studies than this one. REFERENCES: 1. Bjelakovic G, et.al. Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention: Systematic Review and Meta-analysis. JAMA 2007. 297(8):842-857 2. Miller ER 3rd, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med. 2005 Jan 4;142(1):37-46. Epub 2004 Nov 10. Summary for patients in: Ann Intern Med. 2005 Jan 4;142(1):I40. PMID: 15537682 3. Hathcock JN, et al. Vitamins E and C are safe across a broad range of intakes. Am J Clin Nutr. 2005 Apr;81(4):736-45. Review. PMID: 15817846 4. Levin, N. Land of Confusion: How Poor Science and Misleading Media Coverage Create Public Confusion About How Dietary Supplements Affect Health. J App Nutr, Vol 55, No. 1, 2005 8-15 5. Beckman KB, Ames BN. The free radical theory of aging matures. Physiol Rev. 1998 Apr;78(2):547-81. Review. PMID: 9562038 6. BLOCK, G. Are clinical trials really the answer? Am. J. Clin. Nutr. 62, Suppl.: 15175-15205, 1995 7. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med. 1994 Apr 14;330(15):1029-35. http://content.nejm.org/cgi/content/full/330/15/1029?ijkey=bd47b716724d0dad4cad0fb19337308753658337 8. Wright ME, et al. Development of a Comprehensive Dietary Antioxidant Index and Application to Lung Cancer Risk in a Cohort of Male Smokers. July 2004 American Journal of Epidemiology http://aje.oupjournals.org/cgi/content/abstract/160/1/68?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&andorexacttitleabs=and&fulltext=beta+carotene&andorexactfulltext=and&searchid=1100534768534_1530&stored_search=&FIRSTINDEX=0&sortspec=relevance&fdate=7/1/2004&tdate=7/31/2004&journalcode=amjepid 9. Buijsse B, et al. Plasma carotene and alpha-tocopherol in relation to 10-y all-cause and cause-specific mortality in European elderly: The Survey in Europe on Nutrition and the Elderly, a Concerted Action (SENECA). Am J Clin Nutr 2005;82:879–886. 10. Brighenti F. The total antioxidant capacity of the diet is an independent predictor of plasma beta-carotene. European Journal of Clinical Nutrition (2007) 61, 69–76. 11. Clark LC, Marshall JR. Randomized, controlled chemoprevention trials in populations at very high risk for prostate cancer: elevated prostate-specific antigen and high-grade prostatic intraepithelial neoplasia, Urology 57 (2001), pp. 185–187. 12. Duffield-Lillico, AJ, et al. Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: a summary report of the Nutritional Prevention of Cancer Trial, Cancer Epidemiol. Biomarkers Prev. 11 (2002), pp. 630–639. 13. Stampfer MJ, et al. Vitamin E consumption and the risk of coronary disease in women. N Engl J Med 1993;328:1444-9 14. Bauernfeind, J. Tocopherols in Foods. In: Vitamin E: A Comprehensive Treatise. Marcel Dekker, Inc., New York and Basel, pp. 99-167, 1980. 15. Horwitt, M.K. The Promotion of Vitamin E. J. Nutr. 116:1371-1377, 1986. 16. Weber, P., Bendich, A. and Machlin, L.J. Vitamin E and Human Health: Rationale for Determining Recommended Intake Levels. Nutrition 13:450-460, 1997. 17. I-Min Lee, MBBS, ScD; et al. Vitamin E in the Primary Prevention of Cardiovascular Disease and Cancer. The Women’s Health Study: A Randomized Controlled Trial. JAMA. 2005;294:56-65 18. Meydani SN, et al. Vitamin E and respiratory tract infections in elderly nursing home residents: a randomized controlled trial. JAMA. 2004 Aug 18;292(7):828-36. Erratum in: JAMA. 2004 Sep 15;292(11):1305. PMID: 15315997 19. Narayanan BA. Chemopreventive agents alters global gene expression pattern: predicting their mode of action and targets. Curr Cancer Drug Targets. 2006 Dec;6(8):711-27. Review. PMID: 17168675 20. Valko M, et al. Free radicals and antioxidants in normal physiological functions and human disease. Int J Biochem Cell Biol. 2007;39(1):44-84. Epub 2006 Aug 4. Review. PMID: 16978905 21. Chiu CJ, Taylor A. Nutritional antioxidants and age-related cataract and maculopathy. Exp Eye Res. 2007 Feb;84(2):229-45. Epub 2006 Jul 31. Review. PMID: 16879819 22. Moriarty-Craige SE, et al. Antioxidant supplements prevent oxidation of cysteine/cystine redox in patients with age-related macular degeneration. Am J Ophthalmol. 2005 Dec;140(6):1020-6. PMID: 16376645 23. Richer S, et al. Double-masked, placebo-controlled, randomized trial of lutein and antioxidant supplementation in the intervention of atrophic age-related macular degeneration: the Veterans LAST study (Lutein Antioxidant Supplementation Trial). Optometry. 2004 Apr;75(4):216-30. PMID: 15117055 24. Koh HH, et al. Macular Pigment Optical Density in Early, Age-Related Maculopathy (ARM); Comparisons With Normals and Effects of a Lutein Supplement. Invest Ophthalmol Vis Sci 2002; 43:2562 25. Meyer CH, Sekundo W. Nutritional supplementation to prevent cataract formation. Dev Ophthalmol. 2005;38:103-19. Review. PMID: 15604620 26. DaVanzo JE, et al. An Evidence-Based Study of the Role of Dietary Supplements in Helping Seniors Maintain their Independence. The Lewin Group Inc. January 20, 2006 27. National Institutes of Health, Institute of Medicine, Office of Dietary Supplements. Vitamin E Fact Sheet

Another Decade of AIDS (HIV)

In 1995 a protocol for nutritional support of people who were HIV positive was published by a nutrition group headed by Willis H. Reisen, PhD, who received his PhD in biochemistry from the University of Wisconsin in the 1950's and was board certified as a clinical nutritionist in the early 1990's. Dr. Reisen, and his colleague David B. Tardy, self-published their short pamphlet, A Decade of AIDS, after a ten-year period during which they claimed that not a single one of the approximately one hundred HIV-positive people following this protocol had gone from HIV-positive to full-blown AIDS. (Both of these good gentlemen have since passed away at a ripe age.)

I am providing the recommendations of their original protocol in a very short form largely for historical purposes, but also to open people's minds to the possibilities of using nutrition to complement conventional medical care. I'm also providing independent scientific references that I have dug up to document the current science backing up their original protocol, which I present below.

A bit of explanation of the supplemental options was also added by me, along with a few examples of modern formulas providing these nutrients more efficiently than those available on the market some 10-12 years ago.

Please remember that this protocol was designed to be used under a physician's care, and should NOT be used as a substitute for medical care!

HIV nutritional support protocol (to be used only under the medical supervision of a physician):

This protocol has traditionally (since 1985) been used by some clinical nutritionists for the nutritional support of people with HIV for nutritional restoration of the digestive and immune systems. Use this protocol only as directed by your physician.

Nutritional Protocol:

• Probiotics include acidophilus, bifidus, and other ‘beneficial bacteria’ that are healthy for the human gut. If you are not using an antibiotic prescription drug, simply take a good quality, strong probiotic formula as directed on the label. If you are currently taking an antibiotic prescription drug, supplement with a good quality, strong probiotic formula an hour or two after each dose of antibiotic, then continue taking the probiotics for some weeks after the antibiotic course is over.
• Take a good hi-potency multiple vitamin to provide basic nutritional supplementation.1, 2, 17-33, 45
• Take antioxidants to increase detoxification and glutathione production. Cysteine or NAC 3,4, whey protein isolate 34-36, GliSODin ™ 37, 39-44 Silymarin (milk thistle extract) VitaBerry™ or other hi-ORAC antioxidant formula Selenium, preferably selenomethionine, 200-400 mcg/day. 5-8, 39
• Do a Vitamin C flush, maintaining appropriate levels: http://www.askrph3.com/healthcare/article_cflush.shtml 9-11, 38
• Natural carotenoids 46-48 AIDS-related weight loss and chronic diarrhea ("HIV enteropathy") may respond to a gluten-free diet. 12
• Progressive resistance training (weight training) and exercise may be used as an alternative or adjunct to steroids. 13,14
• DHEA may alleviate fatigue and depression (200-500 mg per day for eight weeks). DHEA supplementation had no effect on CD4 cell (helper T-cell) counts or testosterone levels. 15,16

References
1. Ince S. Vitamin supplements may help delay onset of AIDS. Med Tribune 1993;9:18.
2. Fawzi WW, Msamanga G, Hunter D, et al. Randomized trial of vitamin supplements in relation to vertical transmission of HIV-1 in Tanzania. J Acquir Immune Defic Syndr 2000;23:246–54.
3. Roederer M, Staal FJ, Raju PA, et al. Cytokine-stimulated human immunodeficiency virus replication is inhibited by N-acetyl-L-cysteine. Proc Natl Acad Sci 1990;87:4884–8.
4. Herzenberg LA, De Rosa SC, Dubs JG, et al. Glutathione deficiency is associated with impaired survival in HIV disease. Proc Natl Acad Sci 1997;94:1967–72.
5. Baum MK, Shor-Posner G, Lai S, et al. High risk of HIV-related mortality is associated with selenium deficiency. J Acquir Immune Defic Syndr Hum Retrovirol 1997;15:370–4.
6. Olmsted L, Schrauzer GN, Flores-Arce M, Dowd J. Selenium supplementation of symptomatic human immunodeficiency virus infected patients. Biol Trace Elem Res 1989;25:89–96.
7. Chariot P, Perchet H, Monnet I. Dilated cardiomyopathy in HIV-infected patients [letter; comment]. N Engl J Med 1999;340:732 (discussion 733–5).
8. Zazzo JF, Lafont A, Darwiche E, et al. Is non-obstructive myocardiopathy (NOMC) in AIDS selenium-deficiency related? In: Neve J, Favier A, eds. Selenium in biology and medicine. W. DeGruyter & Co.: Berlin New York, 1988, 281–2.
9. Harakeh S, Jariwalla RJ, Pauling L. Suppression of human immunodeficiency virus replication by ascorbate in chronically and acutely infected cells. Proc Natl Acad Sci 1990;87:7245–9.
10. Tang AM, Graham NMH, Saah AJ. Effects of micronutrient intake on survival in human immunodeficiency type 1 infection. Am J Epidemiol 1996;143:1244–56.
11. Cathcart RF III. Vitamin C in the treatment of acquired immune deficiency syndrome (AIDS). Med Hypotheses 1984;14:423–33.
12. Nellen H, Flores G, Wacher N. Treatment of human immunodeficiency virus enteropathy with a gluten-free diet. Arch Intern Med 2000;160:244 [letter].
13. Roubenoff R, McDermott A, Weiss L, et al. Short-term progressive resistance training increases strength and lean body mass in adults infected with human immunodeficiency virus. AIDS 1999;13:231–9.
14. Mustafa T, Sy FS, Macera CA, et al. Association between exercise and HIV disease progression in a cohort of homosexual men. Ann Epidemiol 1999;9:127–31.
15. Ferrando SJ, Rabkin JG, Poretsky L. Dehydroepiandrosterone sulfate (DHEAS) and testosterone: relation to HIV illness stage and progression over one year. J Acquir Immune Defic Syndr 1999;22:146–54.
16. Rabkin JG, Ferrando SJ, Wagner GJ, Rabkin R. DHEA treatment for HIV + patients: effects on mood, androgenic and anabolic parameters. Psychoneuroendocrinology 2000;25:53–68.
17. Semba RD, Graham NMH, Caiaffa WT, et al. Increased mortality associated with vitamin A deficiency during human immunodeficiency virus type 1 infection. Arch Intern Med 1993;153:2149–54.
18. Semba RD, Miotti PG, Chiphangwi JD, et al. Maternal vitamin A deficiency and mother-to-child transmission of HIV-1. Lancet 1994;343:1593–7.
19. Coutsoudis A, Pillay K, Spooner E, et al. Randomized trial testing the effect of vitamin A supplementation on pregnancy outcomes and early mother-to-child HIV-1 transmission in Durban, South Africa. South African Vitamin A Study Group. AIDS 1999;13:1517–24.
20. Kennedy CM, Coutsoudis A, Kuhn L, et al. Randomized controlled trial assessing the effect of vitamin A supplementation on maternal morbidity during pregnancy and postpartum among HIV-infected women. J Acquir Immune Defic Syndr 2000;24:37–44.
21. Fawzi WW, et al. (2004). A randomized trial of multivitamin supplements and HIV disease progression and mortality. N Engl J Med 351, 23–32
22. Coutsoudis A, Bobat RA, Coovadia HM, et al. The effects of vitamin A supplementation on the morbidity of children born to HIV-infected women. Am J Public Health 1995;85:1076–81.
23. Kanter AS, Spencer DC, Steinberg MH, et al. Supplemental vitamin B and progression to AIDS and death in black South African patients infected with HIV. J Acquir Immune Defic Syndr 1999;21:252–3 [letter].
24. Butterworth RF, Gaudreau C, Vincelette J, et al. Thiamine deficiency in AIDS. Lancet 1991;338:1086.
25. Baum MK, Mantero-Atienza E, Shor-Posner G, et al. Association of vitamin B6 status with parameters of immune function in early HIV-1 infection. J Acquir Immune Defic Syndr 1991;4:1122–32.
26. Tang AM, Graham NMH, Saah AJ. Effects of micronutrient intake on survival in human immunodeficiency type 1 infection. Am J Epidemiol 1996;143:1244–56.
27. Boudes P, Zittoun J, Sobel A. Folate, vitamin B12, and HIV infection. Lancet 1990;335:1401–2.
28. Murray MF. Niacin as a potential AIDS preventive factor. Med Hypotheses 1999;53:375–9.
29. Murray MF, Srinivasan A. Nicotinamide inhibits HIV-1 in both acute and chronic in vitro infection. Biochem Biophys Res Commun 1995;210:954–9.
30. Tang AM, Graham NMH, Saah AJ. Effects of micronutrient intake on survival in human immunodeficiency type 1 infection. Am J Epidemiol 1996;143:1244–56.
31. Graham NMH, Saah AJ. Effects of micronutrient intake on survival in human immunodeficiency type 1 infection. Am J Epidemiol 1996;143:1244–56.
32. Fabris N, Mocchegiani E, Galli M, et al. AIDS, zinc deficiency, and thymic hormone failure. JAMA 1988;259:839–40.
33. Mocchegiani E, Veccia S, Ancarani F, et al. Benefit of oral zinc supplementation as an adjunct to zidovudine (AZT) therapy against opportunistic infections in AIDS. Int J Immunopharmacol 1995;17:719–27.
34. Micke P, Beeh KM, Buhl R. Effects of long-term supplementation with whey proteins on plasma glutathione levels of HIV-infected patients. Eur J Nutr 2002;41:12–8.
35. Wong KF, Middleton N, Montgomery M, et al. Immunostimulation of murine spleen cells by materials associated with bovine milk protein fractions. J Dairy Sci 1998;81:1825–32.
36. Minehira K, Inoue S, Nonaka M, et al. Effects of dietary protein type on oxidized cholesterol-induced alteration in age-related modulation of lipid metabolism and indices of immune function in rats. Biochim Biophys Acta 2000;1483:141–53.
37. Muth CM, Glenz Y, Klaus M, Radermacher P, Speit G, Leverve X. Sektion. Influence of an orally effective SOD on hyperbaric oxygen-related cell damage. Free Radic Res. 2004 Sep;38(9):927-32. PMID: 15621710
38. Stephensen CB, et al. Vitamins C and E in adolescents and young adults with HIV infection. Am J Clin Nut. Vol. 83, No. 4, 754-759, April 2006
39. Foster HD. How HIV-1 causes AIDS: implications for prevention and treatment. Med Hypotheses. 2004;62(4):549-53. Review. PMID: 15050105
40. The effects of an orally effective SOD (Glisodin) on AIDS West African patients in a randomized double-blinded clinical study. http://www.health-strategy.com/contentmgr/showdetails.php/id/3787
41. Dugas B (2002) Glisodin®, a nutraceutical product that promotes the oral delivery of superoxide dismutase. Free Radic Biol Med 33: S64
42. Vouldoukis I, Conti M, Kolb JP, et al.(2003) Induction of Th1-dependent immunity by an orally effective melon superoxide dismutase extract. Curr Trends Immunol 5: 141-5
43. Vouldoukis I, Conti M, Krauss P, et al. (2004) Supplementation with gliadin-combined plant superoxide dismutase extract promotes antioxidant defences and protects against oxidative stress. Phytother Res 18 (12): 957-62
44. Vouldoukis I, Lacan D, Kamate C, et al. (2004) Antioxidant and anti-inflammatory properties of a Cucumis melo LC. extract rich in superoxide dismutase activity. J Ethnopharmacol 94 (1): 67-75
45. Jiamton S, et al. (2003). A randomized trial of the impact of multiple micronutrient supplementation on mortality among HIV-infected individuals living in Bangkok. AIDS 17, 2461–2469
46. Austin J. A community randomized controlled clinical trial of mixed carotenoids and micronutrient supplementation of patients with acquired immunodeficiency syndrome. Eur J Clin Nutr 60: 1266-1276; advance online publication, May 24, 2006; doi:10.1038/sj.ejcn.1602447
47. Baum MK, Shor-Posner G, Lu Y, Rosner B, Sauberlich HE, Fletcher MA et al. (1995). Micronutrients and HIV-1 disease progression. AIDS 9, 1051–1056 48. Stephensen CB (2003). Vitamin A, beta-carotene, and mother-to-child transmission of HIV. Nutr Rev 61, 280–284