Sunday, March 23, 2014

Are vitamin and mineral supplements a waste of money? By Jerry Brainum

An article published in the December 17, 2013 issue of the Annals of Internal Medicine made the bold claim that vitamin-mineral supplements are a waste of money for most people. The article authors noted that the evidence that vitamins and minerals have any preventive effect against the onset of the major killer diseases, including cardiovascular disease and cancer, is scant to non-existent. Furthurmore, asserts the doctors who wrote the article, vitamins and minerals will do nothing to help you live longer. Of course, since so many people, even those who aren't into using food supplements, still ingest a basic vitamin and mineral formulation as "nutritional insurance," this story merited being picked up by the popular media, who preceded to produce stories with such headlines as "Vitamin and minerals are worthless and a waste of money."
   However, as is typical with popular science reporting, several important points were not mentioned in the Internet and newspaper reports. For one, the assumption of the medical journal article was that most people are consuming enough nutrients in food, and therefore don't need any supplements. This further makes the assumption that most people consume a balanced diet that is replete in all necessary nutrients. That notion is nothing less than a fantasy on the part of the medical journal authors. Had they bothered to look at the latest government nutritional surveys, they would quickly have noted that the majority of Americans are in fact, not even meeting the minimal suggested daily intake of many vitamins and minerals.
   One reason for this is the reliance on processed and fast foods, which are devoid of many essential nutrients, but are top-heavy in carbohydrates and fats. Few people consume even the minimal suggested intake of five servings a day of fruits and vegetables, and without eating these foods, they will not be getting some of the essential nutrients. The obvious question is: if they aren't obtaining these required nutrients from food sources, where are they getting them? The answer is no where. And contrary to what was wrongly stated in the medical journal article, a long-term lack of nutrients is indeed linked to disease onset, even if it involves just a nutrient deficiency.
    The authors also overlooked individual requirements for certain nutrients. The concept of biochemical individuality states that, due to certain slight gene differences, some nutrients may be more required than others in some people. One example of this involves the production of a byproduct of amino acid metabolism called homocysteine . Homocysteine is produced from the metabolism of the essential amino acid, methionine. Normally, the body deals with it without a problem. But in some people, again likely due to slight genetic differences, homocysteine can accumulate in the body. When this happens, a few toxic effects may accrue. This includes acceleration of both cardiovascular disease and brain degeneration. The good news is that homocystine is capable of being broken down into harmless substances, as long as three nutrients are present: vitamins B6, B12, and folic acid. If a person who overproduces homocysteine isn't consuming enough of these three nutrients from food sources, eventual health disaster is likely.
    Then there is the case of the obese. Studies show that those with high body fat levels tend to sequester nutrients in their body fat, where the nutrients are inert. This is particularly true of the fat-soluble class of vitamins, such as vitamins E and D. In fact, studies conclusively show that obese people need to ingest higher doses of vitamin D just to reach an optimal blood level of the nutrient. A recent study examined the nutrient intake of obese subjects, both before and after being placed on special weight-reduction plan. This plan was designed to deliver all required vitamin and minerals in optimal amounts for health promotion. In fact, the plan actually delivered a level of vitamins and minerals that was slightly above suggested intakes.
     Prior to starting the special diet plan, the obese people were examined for any pre-existing nutrient deficiencies. This revealed deficiencies for vitamin D, vitamin C, selenium, iron, beta-carotene, and lycopene. The researchers conducting the study determined this by taking buccal or inner cheek smears from the subjects, since this method was more reflective of nutrient uptake and long-term intake of the nutrients, rather than a blood sample, which would just provide a more immediate picture.
   As noted, these obese subjects were placed on a special formula diet that at its strictest phase, provided only 800 calories a day. But they also were provided enough protein and other nutrients to prevent any problems.Despite this, while on the formula diet for three months, the obese subjects still showed deficiencies of vitamin C, selenium, iron, zinc, and lycopene. And this was true despite the fact that they were supplied these nutrients based on suggested daily requirements. So why were they still deficient?
    When losing fat in large quantities, the level of oxidation in the body increases significantly. As such, the minimal level of nutrients that the subjects ingested, most of which were antioxidants, were being used up to decrease the potentially dangerous byproducts of increased oxidation from the fat utilization.In addition, the fat-soluble vitamins, instead of being circulated in the blood, were instead shunted into fat reserves, which not only neutralized their effectiveness, but also increased the oxidation effect. The fat cells also exert an inflammatory effect, which adversly affects iron metabolism by boosting levels of hepcidin, a substance that controls iron uptake into the body.
   So, as this study shows, obese people show a definite increased need for certain vitamins and minerals that is above the recommended suggested intake of these nutrients. This is particularly true under dieting conditions, when increased oxidation effects will use up existing levels of minimal vitamins and minerals in the blood. Also, the fat sequestration effect must also be considered. Obese people need to ingest higher amounts of fat-soluble vitamins to get the same protective effects as their leaner peers.
    The absolute stupidity of suggesting that vitamin-mineral supplements are a waste of money is obvious. For the tiny minority of people that truly do ingest a balanced diet, they aren't as necessary, unless there is a genetic quirk that demands higher intake of certain nutrients. For all the rest, vitamins and mineral supplements can represent the difference between long-term health and disease. The salient question really comes down to this: Who stands to gain if people stop ingesting vitamins and minerals, and eventually become afflicted with health problems related to the lack of those nutrients?


Damms-Machado, A, et al. Micronutrient deficiency in obese subjects undergoing low calorie diet.Nutrition Journal 2012;11;34.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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Tuesday, March 4, 2014

Does a higher protein intake increase the risk of death? by Jerry Brainum

High protein diets have always been controversial. Critics of the diets often predict dire consequences for those foolish enough to stay on such diets long-term.These consequences include kidney disease and bone mass loss. However, more recent analysis of such possible risks show that they exist more on paper than in reality. When examined in healthy, active adults, higher protein intakes have consistently been shown not to impose any undue risks on kidney function, bone mass, or other factors. Athletes and others engaged in regular physical activity have long been advised to ingest a higher protein intake. In some cases, the level of protein intake is extreme. Some bodybuilders have stated that they regularly ingest as much as 600 grams of protein a day. It's doubtful that this degree of protein intake contributes anything useful to their goal of boosting muscle mass. Most excess protein is merely degraded and oxidized in the liver.
    But two alarming new studies, both published in the March 4, 2014 issue of the journal, Cell Metabolism, assert that a higher protein intake is not only not necessary,but could shorten lifespan if consumed during middle-age. The first study analyzed data from a nationwide nutrition study, and specifically looked at the protein intake of 6,831 middle-aged adults.The data showed that adults with an average age of 50 who consumed a diet that contained more than 20% of calories as protein were 4-times more likely to die of cancer or diabetes, and more than twice as likely to die from any cause in the next 18 years. Even a moderate protein diet of 10 to 19% protein was still associated with a 3-fold increase in death from cancer. Interestingly, the effect was only associated with consumption of animal proteins. Consuming protein from plant sources, such as beans, did not result in any negative effects on health. Even more intriguing was the finding that this effect was reversed in people over age 65; that is, those consuming a higher protein diet showed a 28% reduced risk of mortality from any cause, and a 60% reduced risk of dying from cancer. The effects of consuming a higher protein diet during middle-age on mortality were comparable to smoking!
     This, of course, is very bad news for anyone who ingests a high protein diet, especially those who are middle-age. But let's take a closer look at these findings. What, for example, is it about a high protein diet that seems to increase mortality? According to the study authors, the likely explanation is that a high protein (and higher calorie) diet boosts levels of a hormone called Insulinlike growth-factor-1 or simply, IGF-1. IGF-1 is produced both locally in muscle, where it functions as a major arbiter of promoting muscle growth, and in the liver, where it provides systemic body effects. These effects include helping to preserve lean mass, bone, neurons in the brain, and heart muscle. Without sufficient IGF-1, these tissues and organs degenerate. But IGF-1 has also been implicated in the cancer process because it promotes mitosis, or cellular division. Cancer involves uncontrolled cell division. But scientists still quibble over the precise role that IGF-1 plays in cancer. Among other effects, IGF-1 prevents a process called apoptosis, a type of cellular suicide. One theory suggests that tumors upgrade local IGF-1 synthesis as means of survival.Other theories say that it's the circulating IGF-1 itself that promotes cancer spread. On the other hand, IGF-1 travels in the blood bound to six different binding proteins, with IGFBP-3 being the predominant form. An important point is that IGF-1 can only interact with cells when it is unbound, or free. Bound IGF-1 is basically inert.So the question then arises: what can cause IGF-1 to be released from its binding protein? One thing that does this is insulin, as well as estrogen. When these two hormones are released in greater amounts in the blood, you also get a higher level of free IGF-1, which may be capable of interacting with existing tumors.
   An important point to consider about this new study is that no mention is made of what other nutrients the subjects ingested. If they had excess bodyfat, which is linked to higher levels of estrogen, that would account for their elevated IGF-1 levels. If they consumed excess carbohydrates, and were also pre-diabetic, this, too, would lead to higher free IGF-1 levels. The study authors implicated protein because protein is known to boost IGF-1 levels, but not necessarily the free or active form. But the mere fact that the data was derived from an epidemiological survey brings the findings into question, since such surveys are notoriously unreliable.    
    The study authors note that mice on restricted protein diets show a 45% decrease in tumor mass after two months. But they also say that consuming a higher protein diet protects people over age 65. This relates to the prevention of frailty associated with a lack of IGF-1, which is a major cause of death in older people. Yet, who has the highest rates of cancer? People over age 65. So why would a high protein diet, which is known to boost IGF-1, lead to less mortality in the older people? According to the study authors' suggestion, the higher IGF-1 induced by a higher protein intake should result in a greater incidence of cancer in an older population, especially since such older people usually have an abundance of damaged DNA in their cells--a scenario highly favorable to cancer onset. Would this same information apply to active people, who use or metabolize a higher protein intake differently compared to those who are sedentary?
   The other study exclusively used mice as subjects, and found that a low protein, high fat diet was most detrimental to health. But they also found that a very high carbohydrate intake of 70% of ingested calories, along with a low protein intake, was most conducive to longevity!  The most surprising aspect of the study, however, was the finding that reducing calories had no effect on longevity. This is contrary to dozens of previously published studies, which did find increased lifespan among various species who ingested a lower caloric intake. On the other hand, the stated mechanism for the increase in longevity linked to the high carb, low protein diet was a decrease in mTOR. mTOR is a protein that is crucial to protein synthesis, and is increased by a higher protein intake. But it is also associated with faster aging and spread of cancer in later years. But mTOR can easily be controlled by far less extreme measures than restricting protein while shoveling in high amounts of carbohydrates. The latter is disastrous for the estimated 50 million Americans who have insulin insensivity or "pre-diabetes," and would, without a doubt, result in an increase in mortality, rather than longevity, if ingested. The study authors did note that the mice who consumed a low protein, high carb diet not only consumed far more calories, but were also significantly fatter than mice who consumed a higher protein, lower carb intake. How being fat and overeating can boost lifespan is a type of metabolic magic that I doubt that anyone can explain, but it may work for mice, certainly not for humans!

©,2014 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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