Food Manufacturers Are Fooling You

By Mike Sheridan

Fact: The unhealthiest foods you could possibly eat often have the most health claims on the label. Ironic, isn't it? Think about most breakfast cereals. You're basically eating a bowl of sugar and flour. But the front of the box is packed with health claims:

  • Low fat!
  • Heart healthy!
  • High fiber!
  • Gluten-free!
  • Reduced sodium!
  • Made with whole grains!

Flip that box around like a smart grown-up and take a look at the ingredient list: sugar, flour, sugar in another form, sugar in a different color, sugar with a pretty name, etc. It's Type-2 diabetes in a bright box featuring a cartoon character selling love handles and loneliness.

And now they have a new marketing angle: a clever blend of childhood nostalgia and "fat acceptance." They tell us to eat what we want and love our body no matter what it looks like. Presumably, this is because they've finally recognized that the only people still eating cereal for breakfast have already given up on their health and body composition.

Funny thing is, when looking at the evidence, it's clear that there were never really health benefits in the first place to back up all these "healthy" labels. Here's how many of them originated and why they're wrong.

1 – Low Fat

It's taken over 40 years to officially call BS on the fraudulent claims about fat. The fear of dietary fat started in the 60's and 70's and immediately moved breakfast cereal into the "healthy" category. Hey, sugar is fat free! Bacon, eggs, and butter were out. Low-fat indigestible roughage was in because the research of the time was suggesting that saturated fat was clogging our arteries and increasing our risk of heart disease.

And despite the various top-notch review studies disproving this myth today, the cereal killers, sugar-water sellers, and big pharma phonies continue to lobby government officials, pay off medical and fitness professionals, and fund bogus research studies to keep it alive.

A low-fat diet isn't a benefit because eating fat doesn't cause disease. NOT eating it probably does, and we now know the body even needs some saturated fat to function optimally.

2 – High Fiber

Once you understand the origins of the low-fat guidelines it's easy to see how the advice to eat more fiber came about.

Denis Burkitt was the man behind the 1970's research linking high-fiber diets to lower rates of disease (colorectal cancer specifically). Just like Ancel Keys (the fat fraud), his evidence was awful. He basically claimed that African tribesman were healthier than Westerners because they ate their grains whole (with the fibrous outer shell). He conveniently failed to include a number of disease-free tribes thriving on starch-less diets high in saturated fat and animal protein, like the Masai.

Nonetheless, the bran we were throwing in the garbage became a prized possession, Burkitt wrote a best-selling book, and the "high-fiber" stamp fit perfectly next to the "low-fat" one on our breakfast bowl of blood sugar and body fat. It remains there today, right along with the misconception that whole grains are healthier than refined grains and that more fiber is a good thing, regardless of the source.

Meanwhile, the only study looking at the long-term impact of eating a high-fiber diet (DART, 1989) found an INCREASED risk of heart disease (23%) and mortality (27%). Those studies looking at colorectal cancer saw no benefit to upping our fiber intake:

"Our data do not support the existence of an important protective effect of dietary fiber against colorectal cancer or adenoma." (Fuchs CS et al. NEJM, 1999)

"In this large pooled analysis... high dietary fiber intake was not associated with a reduced risk of colorectal cancer." (Park Y et al. JAMA, 2005.)

3 – Cholesterol

The "lipid hypothesis" suggests that elevated cholesterol is associated with heart disease. And when we add it to what high-fiber, low-fat fanatics tell us, it's no wonder we think the way we do and fall for bogus health claims.

Right around the time all this low-fat, high-fiber evidence was surfacing, doctors and scientists were convinced they'd found the underlying cause of atherosclerosis – the narrowing and hardening of arteries. Nearly every doctor was on board with the theory. In the early 80's the National Institute of Health gathered 14 experts who voted unanimously that, "Lowering elevated blood cholesterol levels will reduce the risk of heart attacks caused by coronary heart disease."

They did so despite the fact that a causal relationship was never established, there's a library of evidence disproving it, and the original experiments used rabbits (herbivores that can't process dietary cholesterol) and a chemically prepared bare-cholesterol, which tends to oxidize.

But along came the prescription statins, and all of a sudden the questions and doctors aggressively opposing the theory disappeared. This created an environment where we dish out damaging side effects to more than 32 million Americans to lower the thing that's NOT associated with heart disease and does nothing to prevent it.

If cholesterol were associated with heart disease, there would be fewer heart attacks in those on statins and those with lower cholesterol, but there aren't. And there would be more heart attacks in those not on statins with higher cholesterol, but there aren't. The two variables aren't even related.

What we do see is statins causing mitochondrial and hormonal dysfunction, and lower cholesterol levels associated with cognitive and neurological impairment (Alzheimer's, Parkinson's, depression). This shouldn't come as a surprise when you understand that cholesterol is a building block for cell membranes, precursor to steroid hormones and essential nutrients, and fuel provider to neurons who can't generate it on their own.

"Our finding that low plasma cholesterol is associated with depressive symptoms in elderly men is compatible with observations that a very low total cholesterol may be related to suicide and violent death." (Morgan RE, et al. 1993, Lancet.)

Cereal fiber's ability to lower cholesterol is more of a detriment than a benefit. And realistically, the people getting heart attacks are the ones with elevated triglycerides, low HDL cholesterol, and excess small-dense (oxidizable) LDL particles – the same thing eating less saturated fat, more high-glycemic carbs, and vegetable oil-filled boxes of stuff claiming to "lower cholesterol" provides.

4 – Sodium

Heard the one about the obese, pre-diabetic guy with high triglycerides? Doc told him to eat less salt!

That's a joke. Or at least it should be. Salt doesn't make you fat and it's probably the last thing the average person needs to be worrying about when it comes to health.

High blood pressure is the fourth and final phase that turns Syndrome X into the Deadly Quartet. When you have metabolic syndrome, eating less salt won't do anything to solve the real problem.

  • 2 weeks – insulin resistance (hyperinsulinemia)
  • 2 months – elevated triglycerides (hyperlipidemia)
  • 6 months – obesity (high bodyfat)
  • 12 months – high blood pressure (hypertension)

People with high blood pressure don't need to eat less salt. They need to stop drinking liquid fructose and start driving-past instead of driving-thru.

More importantly, trying to abide by the FDA and AHA's recommendations to keep salt intake below 2400 mg per day (1tsp) increases cardiovascular disease risk and mortality from a heart attack or stroke. Ironically, this appears to be the result of elevated triglycerides and reductions in insulin sensitivity – the same thing driving the high blood pressure in the first place.

"The inverse association of sodium to CVD mortality seen here raises questions regarding the likelihood of a survival advantage accompanying a lower sodium diet." (Cohen HW, et al. AJM, 2006)

Therefore, one could say that your low-salt food is a double-whammy since you're consuming the food that's elevating the cause of high blood pressure and opting for the "lowers blood pressure" variety that's making it worse.

5 – Gluten

The gliadin proteins in wheat can be damaging to many people because of those proteins' ability to induce inflammation and increase intestinal permeability. Wheat itself may also cause cravings and interfere with your appetite-regulating mechanisms.

However, this doesn't mean all products with a "gluten-free" stamp of approval are suddenly health foods. Pizza is still pizza, pancakes are still pancakes, and a slab of pound cake beside your coffee is and always will be a bad choice... gluten-free or not. This should be common sense, but millions are willingly fooled every day because it's pretty easy to convince us that a delicious junk food is fine when it has an official-looking health claim on the box.

Just like we were tricked into selecting low-fat and low-sodium packaged products because of their apparent health benefit, food marketers have simply found another way to convince you that their bag or box of garbage is healthy.

Gluten-free cereal may be better than gluten-filled cereal, but it's still cereal. And you'd be better off leaving both for the birds.

References

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  3. Skeaff CM and Miller J. 2009. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab 55(1-3):173-201.
  4. Yamagishi K, et al. 2010. Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. Am J Clin Nutr 92(4):759-65.
  5. Mente A, et al. 2009. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 169(7):659-69.
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  8. Mann GV, et al. 1971. Atherosclerosis in the Masai. Am J Epidemiol 95 (1): 26-37.
  9. Burr ML, et al. 1989. Diet and reinfarction trial (DART): design, recruitment, and compliance. Eur Heart J 10(6):558-67.
  10. Fuch CS, et al. 1999. Dietary fiber and the risk of colorectal cancer and adenoma in women. N Engl J Med 340(3):169-76.
  11. Park Y, et al. 2005. Dietary Fiber Intake and Risk of Colorectal Cancer: A Pooled Analysis of Prospective Cohort Studies. JAMA 294(22):2849-2857.
  12. Steinberg D. 2006. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy, part V: the discovery of the statins and the end of the controversy. J Lipid Res 47(7):1339-51.
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  14. Stehbens WE. 2001. Coronary heart disease, hypercholesterolemia, and atherosclerosis. I. False premises. Exp Mol Pathol 70(2):103-19.
  15. Golomb BA and Evans MA. 2008. Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism. Am J Cardiovasc Drugs 8(6):373-418.
  16. Krumholz HM, et al. 1994. Lack of Association Between Cholesterol and Coronary Heart Disease Mortality and Morbidity and All-Cause Mortality in Persons Older Than 70 Years. JAMA 272(17):1335-1340.
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  19. Superko HR, et al. 2002. Small LDL and its clinical importance as a new CAD risk factor: a female case study. Prog Cardiovasc Nurs 17(4):167-73.
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  21. Corona G, et al. 2010. The effect of statin therapy on testosterone levels in subjects consulting for erectile dysfunction. J Sex Med 7(4 Pt 1):1547-56.
  22. West R, et al. 2008. Better memory functioning associated with higher total and low-density lipoprotein cholesterol levels in very elderly subjects without the apolipoprotein e4 allele. Am J Geriatr Psychiatry 16(9):781-5.
  23. Huang X, et al. 2008. Low LDL cholesterol and increased risk of Parkinson's disease: prospective results from Honolulu-Asia Aging Study. Mov Disord 23(7):1013-8.
  24. de Lau LM, et al. 2006. Serum cholesterol levels and the risk of Parkinson's disease. Am J Epidemiol 164(10):998-1002.
  25. Shin JY, et al. 2008. Are cholesterol and depression inversely related? A meta-analysis of the association between two cardiac risk factors. Ann Behav Med 36(1):33-43.
  26. Perez-Rodriguez MM, et al. 2008. Low serum cholesterol may be associated with suicide attempt history. J Clin Psychiatry 69(12):1920-7.
  27. Seneff S. 2009. APOE-4: The Clue to Why Low Fat Diet and Statins may Cause Alzheimer's
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  29. Brown L, et al. 1999. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 69(1):30-42.
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  31. Barnard RJ, et al. 1998. Diet-induced insulin resistance precedes other aspects of the metabolic syndrome. J Appl Physiol 84(4):1311-1315.
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  33. Jurgens G and Graudal NA. 2003. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. Cochrane Database Syst Rev 1:CD004022.
  34. Garg R. 2011. Low-salt diet increases insulin resistance in healthy subjects. Metabolism 60(7):965-968.
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  39. Fasano A. 2012. Zonulin, regulation of tight junctions, and autoimmune diseases. Ann N Y Acad Sci 1258(1):25-33.

Grains - The Real Cereal Killer

Watch now/download: https://www.yekra.com/cereal-killers Distribute this film to your audience: http://bit.ly/1kZ1kL2 Synopsis The film follows Donal -- a lean, fit, seemingly healthy 41 year old man -- on a quest to hack his genes and drop dead healthy by avoiding the heart disease and diabetes that has afflicted his family.

By Dr. Mercola

The persistent myth that dietary fat causes obesity and promotes heart disease has undoubtedly ruined the health of millions of people. It's difficult to know just how many people have succumbed to chronic poor health from following conventional low-fat, high-carb recommendations, but I'm sure the number is significant.

In the featured documentary, Cereal Killers, 41-year-old Donald O'Neill turns the American food pyramid upside-down—eliminating sugars and grains, and dramatically boosting his fat intake. In so doing, he improves his health to the point of reducing his hereditary risk factors for heart disease to nil.

Watching people's reactions to his diet brings home just how brainwashed we've all become when it comes to dietary fat. Most fear it. Yet they will consume sugar in amounts that virtually guarantee they'll suffer all the devastating health consequences they're trying to prevent by avoiding fat, and then some!

Fat versus Carbs—What Really Makes You Pack on the Pounds?

The fact is, you've been thoroughly misled when it comes to conventional dietary advice. Most dietary guidelines have been massively distorted, manipulated, and influenced by the very industries responsible for the obesity epidemic in the first place—the sugar and processed food industries.

Shunning the evidence, many doctors, nutritionists, and government health officials will still tell you to keep your saturated fat below 10 percent, while keeping the bulk of your diet, about 60 percent, as carbs.1 This is madness, as it's the converse of a diet that will lead to optimal health.

A recent Time Magazine2 article highlighted a report by the Environmental Working Group (EWG), which showed that many breakfast cereals contain more than 50 percent sugar by weight! Cereals marketed specifically to children are among the worst offenders. Kellogg's Honey Smacks and Mom's Best Cereals Honey-Ful Wheat topped the list with 56 percent sugar by weight. If you're looking for alternatives for your family you could try Snackimals from Barbara's. Snackimals is not on the EWG's list because it is a newer product. All of their flavors have only 7 grams of sugar per serving.

Even diabetes organizations promote carbohydrates as a major component of a healthy diet—even though grains break down to sugar in your body, and sugar promotes insulin resistance, which is the root cause of type 2 diabetes in the first place.

As noted in the film: "If we could get all diabetics to eat a high-fat, high-protein, low-carbohydrate diet, we would cut the insulin requirement so dramatically that it's been estimated that six pharmaceutical companies would go out of business tomorrow."Contrary to popular belief, you do not get fat from eating fat. You get fat from eating too much sugar and grains.

Refined carbohydrates promote chronic inflammation in your body, elevate low-density LDL cholesterol, and ultimately lead to insulin and leptin resistance. Insulin and leptin resistance, in turn, is at the heart of obesity and most chronic disease, including diabetes, heart disease, cancer, and Alzheimer's—all the top killers in the US. 

Don't Fear the Fat

In the film, O'Neill switches over to a diet where 70 percent of his calories come from healthy fat—most of it in the form of macadamia nuts (my personal favorite)—and the remaining 30 percent of his caloric intake is divvied up between protein and fibrous fruits and vegetables. Over the course of 28 days, O'Neill:

  • Loses weight and body fat
  • Increases his lean muscle mass
  • Feels more energetic and improves his athletic performance
  • Increases his resting metabolic rate
  • Improves his blood pressure, cholesterol, and other measurements to the point that he no longer has any risk factors for heart disease, which he's genetically predisposed for

Of particular importance here is that O'Neill's total cholesterol and LDL levels wentup, which initially caused significant concern. However, once they tested the LDL particle numbers, the results showed that his LDL particles were the largest species known, and he had virtually no small LDL particles at all.

This is phenomenal, as it's the small, dense LDL particles that cause inflammation. Large particles do not. Also, the markers for inflammation were virtually nonexistent, showing that he has no inflammation in his body at all. All in all, his one-month long high-fat, no-carb diet experiment proved that:

  • Eating fat helps you lose fat
  • Eating saturated fat decreases your risk factors for heart disease
  • Regardless of your genetic predisposition your diet is, ultimately, the determining factor

I would also add that his results show the benefits of a high-fat, low-carb diet for athletes, many of whom are still convinced that this type of diet will make them heavy and sluggish. On the contrary, O'Neill breaks his own athletic record during his experiment, and refers to his renewed sense of vigor as feeling like a "spring lamb."

This high and sustained energy is a hallmark of ketogenesis, where your body is burning fat rather than sugar as its primary fuel. When your body burns fat, you don't experience the energy crashes associated with carbs.

Saturated Fat and Cholesterol Are Both Necessary for Optimal Health

Contrary to popular belief, saturated fats from animal and vegetable sources provide a number of important health benefits, and your body requires them for the proper function of your:

Cholesterol—another wrongly vilified dietary component—also carries out essential functions within your cell membranes, and is critical for proper brain function and production of steroid hormones, including your sex hormones. Vitamin D is also synthesized from a close relative of cholesterol: 7-dehydrocholesterol. 

Your body is composed of trillions of cells that need to interact with one another. Cholesterol is one of the molecules that allow for these interactions to take place. For example, cholesterol is the precursor to bile acids, so without sufficient amounts of cholesterol, your digestive system can be adversely affected. It's also critical for synapse formation in your brain, i.e. the connections between your neurons, which allow you to think, learn new things, and form memories. In fact, there's reason to believe that low-fat diets and/or cholesterol-lowering drugs may cause or contribute to Alzheimer's disease.3

Replacing Refined Carbs with Healthy Fat—The Answer to Most of Your Health Concerns

Underlying most chronic diseases, including obesity, type 2 diabetes, heart disease, and cancer are inflammation and insulin/leptin resistance. When you eat carbohydrates, your blood sugar, insulin, and leptin will all temporarily rise, and these spikes are very pro-inflammatory. Where you have inflammation, disease and dysfunction follows. An excellent editorial in the journal Open Heart4 reviews the cardiometabolic consequences of replacing saturated fats with carbohydrates, which includes the following:

The answer, then, lies in avoiding these inflammatory spikes in blood sugar, insulin and leptin, and reversing insulin and leptin resistance. To do this, you need to:

  • Avoid refined sugar, processed fructose, and grains. This means avoiding processed foods, as they are chockfull of these ingredients, along with other chemicals that can wreak metabolic havoc
  • Eat a healthful diet of whole foods, ideally organic, and replace the grain carbs you cut out with:
  • Moderate amounts of high-quality protein from organic, grass-fed or pastured animals (this is to ensure you're not getting the antibiotics, genetically engineered organisms, and altered nutritional fat profile associated with factory farmed animals)
  • High amounts of high-quality healthful fat as you want (saturated and monounsaturated). Many health experts now believe that if you are insulin or leptin resistant, as 85 percent of the US population is, you likely need anywhere from 50 to 85 percent of your daily calories in the form of healthful fats for optimal health. Good sources include coconut and coconut oil, avocados, butter, nuts (particularly macadamia), and animal fats. Avoid all trans fats and processed vegetable oils (such as canola and soy oil). Also take a high-quality source of animal-based omega-3 fat, such as krill oil.
  • As many vegetables as you can muster. Juicing your vegetables is a good way to boost your vegetable intake

Another "add-on" suggestion is to start intermittent fasting, which will radically improve your ability to burn fat as your primary fuel. This too will help restore optimal insulin and leptin signaling.

What's the Deal with Protein?

Dr. Rosedale, who was one of my primary mentors on the importance of insulin and leptin, was one of the first professionals to advocate both a low-carb and moderate protein (and therefore high-fat) diet. This was contrary to most low-carb advocates who were, and still are, very accepting of using protein as a replacement for the carbs.

The problem is that, along with grains, most Americans tend to eat far too much protein. While your body certainly has a protein requirement, there's evidence suggesting that eating more protein than your body needs could end up fueling cancer growth.

Dr. Rosedale advises limiting your protein to one gram of protein per kilogram of lean body mass (or 0.5 grams per pound of lean body weight). For most people, this means cutting protein down to about 35-75 grams per day. Pregnant women and those working out extensively need about 25 percent more. I believe this theory is worthy of consideration. The key though is to add healthy fat to replace the carb and protein calories you're cutting out of your diet. Again, sources of healthy fat include:

Your Health Is Within Your Control

Groundbreaking research by the likes of Dr. Robert Lustig and Dr. Richard Johnson (author of the books, The Sugar Fix and The Fat Switch) clearly identifies the root cause of obesity, diabetes, heart disease, and numerous other chronic diseases, and it's notfat. It's refined sugar—particularly fructose—consumed in excessive amounts. Their research, and that of others, provides us with a clear solution to our current predicament. In short, if you want to normalize your weight and protect your health, you need to address your insulin and leptin resistance, which is the result of eating a diet too high in sugars and grains.

For a comprehensive guide, see my free optimized nutrition plan. Generally speaking though, you'll want to focus your diet on whole, ideally organic, unprocessed or minimally processed foods. For the best nutrition and health benefits, you'll also want to eat a good portion of your food raw.

Sugar is highly addictive, and if you're like most people, you're no stranger to carb cravings. Just know that once your body gets used to burning fat instead of sugar as its primary fuel, those cravings will vanish. Many cereals and other grain products would not be quite as harmful if they didn't also contain so much added sugar. Even many organic brands contain excessive amounts. This is unfortunate, since many (Americans in particular) are really indoctrinated to eat cereal for breakfast. I've been working on a low-sugar cereal line for some time now, to provide a healthier alternative for those who really don't want to give up their breakfast cereal. I hope to have it ready sometime this summer.

Last but not least, for those of you still concerned about your cholesterol levels, know that 75 percent of your cholesterol is produced by your liver, which is influenced by your insulin levels. Therefore, if you optimize your insulin level, you will automatically optimize your cholesterol, thereby reducing your risk of both diabetes and heart disease.

Also, remember that even if a high-fat, low-carb diet was to raise your total cholesterol and LDL, it doesn't automatically mean that your diet is increasing your risk factors for heart disease. As O'Neill did in this film, you need to test your LDL particle number. Large-sized particles are good, while the smaller, denser particles can penetrate the lining of your arteries and stimulate the plaque formation associated with heart disease. The former does NOT increase your heart disease risk, while the latter one will. To learn more about LDL particle numbers and how to test them, please see my previous interview with Chris Kresser, L.Ac., which goes into this in some detail.

Too Much Protein??

Media sources often report, “too much protein stresses the kidney.” What does science say? Martin and colleagues reviewed the available evidence regarding the effects of protein intake on kidney function with a particular emphasis on kidney disease. The researchers found: “Although excessive protein intake remains a health concern in individuals with preexisting renal disease, the literature lacks significant research demonstrating a link between protein intake and the initiation or progression of renal disease in healthy individuals.” In addition “At present, there is not sufficient proof to warrant public health directives aimed at restricting dietary protein intake in healthy adults for the purpose of preserving renal function.” Protein restriction is common treatment for people with kidney problems.

 
 

Protein: The Facts, the Myths, and the Real Science

Everyone has an opinion about protein, and the myths surrounding it are rampant. That's why sorting the facts from the crap will lead to better choices regarding your own diet and protein intake. Answer the questions below and see if you've been falling for the myths.

Fact or Myth?

The RDA (Recommended Dietary Allowance) protein suggestions are just fine for people who work out.

Hint: The RDA guideline for protein is 0.8 grams per kilogram of bodyweight per day. So if you weigh 190 pounds (86 kilograms) you'd need about 69 grams of protein.

The Answer: Lifters and athletes concerned with their performance or physique require more protein than what's recommended by the RDA. So it's a myth (and a joke) that the RDA protein recommendations are adequate for ass-kicking individuals.

Here's Why: RDA protein recommendations are too low for certain groups. Those recommendations were never intended for people attempting to enhance performance, maintain, or gain muscle. In fact, a higher protein intake may have positive benefits regarding different health ailments including obesity, type 2 diabetes, osteoporosis, heart disease and muscle wasting.

The RDA guideline reflects the minimum daily needs of protein required to maintain short-term nitrogen balance in healthy, moderately active people. Nitrogen balance compares the amount of nitrogen coming into the body (from dietary protein) to the amount being lost. It's often used as a measurement of protein balance since protein is 16 percent nitrogen.

If you're consuming the same amount of nitrogen that you're losing, you're in nitrogen balance. If you're consuming more than you're losing, you're in positive nitrogen balance. If you're losing more than you're consuming, you're in negative nitrogen balance and are losing protein.

Nitrogen balance studies often involve examining urinary nitrogen levels. Approximately 90 percent of the nitrogen in urine is urea and ammonia salts – the end products of protein metabolism. The remaining nitrogen is accounted for by other nitrogen-containing compounds.

This nitrogen balance method is useful, but it has problems: Urine collections tend to underestimate nitrogen losses, dietary intake tends to be overestimated, miscellaneous skin and hair losses are prone to error, and the response to increased protein intake varies tremendously.

The Really Geeky Stuff

  1. In a review published in the International Journal of Sports Nutrition, researchers concluded, "Those involved in strength training might need to consume as much as 1.6 to 1.7 grams of protein per kilogram per day (approximately twice the current RDA) while those undergoing endurance training might need about 1.2 to 1.6 grams per kilogram per day (approximately 1.5 times the current RDA)."
  2. In another article published in Nutrition & Metabolism, researcher Donald Layman argued that the dietary guidelines should be improved and reflect new understandings about protein requirements. According to him, "During the past decade a growing body of research reveals that dietary protein intakes above the RDA are beneficial in maintaining muscle function and mobility." Diets with increased protein have been shown to improve adult health when it comes to treatment or prevention of obesity, type 2 diabetes, osteoporosis, heart disease and muscle wasting.
  3. A review published in the International Journal of Sport Nutrition and Exercise Metabolism was conducted to evaluate the effects of dietary protein on body composition in energy-restricted resistance-trained athletes, and to provide protein recommendations for these athletes.

The researchers concluded that "...the range of 2.3 to 3.1 grams per kilogram of FFM (fat free mass) is the most consistently protective intake against losses of lean tissue." In other words, for every kilogram on your body that's not fat, you should be consuming 2-3 grams of protein in order to preserve lean tissue. So if you have 190 pounds of lean tissue, up to 258 grams of protein would be optimal for you.

In addition, the goal of the athlete should be considered. Leaner athletes or those having a primary goal of maintaining maximal FFM should aim toward intakes approaching the higher end of this range. Even higher levels of protein than those recommended in the review are not uncommon in exercising individuals. It's unlikely that negative health consequences will follow from higher levels of intake, assuming there are no related health problems that would suggest limiting intake.

Fact or Myth?

The thermic effect of protein is the same as it is for carbs and fat.

Hint: The thermic effect of feeding or diet induced thermogenesis (DIT) is the amount of energy your body has to expend in order to digest and assimilate food. So picture a lean chicken breast (mostly protein), a bowl of rice (mostly carb), and tablespoon of butter (mostly fat). Which do you think your body will have to work hardest to digest?

The Answer: Among the three macronutrients, protein ranks highest in diet induced thermogenesis. So it's a myth that they're all equal in terms of their thermic effect. That means it'll cost you more calories to digest and absorb protein than it would fat and carbohydrate.

Here's Why: The consumption of protein requires an expenditure of 20-30% of the calories derived from protein. So, if 200 calories of protein are eaten, 40-60 calories are burned during digestion. DIT from carbohydrate is 15-20% and 2-5% for fat.

Fact or Myth?

Protein is more satiating (filling) than fat or carbohydrate.

Hints: Protein has an influence on CCK (cholecystokinin) and ghrelin. Protein may stimulate cholecystokinin (CCK) and decrease ghrelin. CCK is secreted mostly from the inner layer of the gastrointestinal tract has been shown to act as a satiety signal. The satiating effect of CCK was first demonstrated when administering CCK to rats. It "dose dependently" reduced meal size. Ghrelin is produced primarily in the stomach and has appetite increasing properties. Ghrelin levels are relatively high prior to a meal and they decrease after a meal.

The Answer: It's a fact that protein is usually more satiating than fat or carbs. When comparing protein, fat, and carbohydrate, protein is generally reported as the most satiating (satisfying to a point of full or beyond) and fat as the least satiating.

Here's Why: Research indicates that one of the primary factors involved with the satiating effects of protein is the thermic effect of feeding, mentioned above. Though protein's influence on ghrelin and CCK may play a large role in its satiating effects, more research needs to be conducted in these areas, as findings have been indecisive. Future research should concentrate on different levels of protein, different types of protein, and consumption of proteins in short and long term.

The Really Geeky Stuff

  1. A review published in Nutrition & Metabolism reported that protein induced thermogenesis has an important effect on satiety. "Protein plays a key role in body weight regulation through satiety related to diet-induced thermogenesis."
  2. A study published in Physiology & Behavior investigated the relative satiating effect of the macronutrients in lean women. On four separate occasions, the composition of an iso-caloric lunch "preload" was controlled in 12 lean women. Macronutrient composition had a significant effect on short-term hunger – the women were less hungry after the protein preload compared to the preloads with the other macronutrients. They also ate less after the protein preload.
  3. A study published in the American Journal of Clinical Nutrition tested the prediction that increasing protein while maintaining the carb content of a diet lowers body weight due to decreased appetite and decreased calorie intake. The study showed when increasing the protein intake from 15% of diet to 30% of diet (while eating the same amount of carbs) there was a decrease in appetite and fewer calories were consumed.
  4. The Journal of Clinical Endocrinology & Metabolism published a study that compared the effect of different proteins and carbohydrates on indicators of appetite and appetite regulatory hormones. CCK level was one of the primary outcomes measured.

Calorie intake was higher after the glucose preload compared with lactose and protein preloads. CCK level was higher 90 minutes after the protein preloads compared with glucose and lactose level. Researchers concluded that "acute appetite and energy intake are equally reduced after consumption of lactose, casein, or whey compared with glucose."

One Quick Caveat

The research sometimes gets a little messy. For example, some studies are indecisive when it comes to protein intake and ghrelin levels. This is why you need to rely on your own reasoning, logic, and experience while gathering info from the research.

References

  1. Blom, A.M., Lluch, A., Stafleu, A., Vinoy, S., Holst, J., Schaafsma, G., & Hendriks, H. (2006). Effect of high-protein breakfast ont he postprandial ghrelin response. The American Journal of Clinical Nutrition, 83(2), 211-220.
  2. Bowen, J., Noakes, M., Trenerry, C., & Clifton, P.M. (2006).Energy intake, Ghrelin, and Cholecystokinin after Different Carbohydrate and Protein Preloads in Overweight Men. The Journal of Clinical Endocrinology & Metabolism, 91(4).
  3. Helms, E., Zinn, C., Rowlands, D.S., & Brown, S.R. (2014). A Systematic Review of Dietary Protein During Caloric Restriction in Resistance Trained Lean Athletes: A Case for Higher Intakes. International Journal of Sport Nutrition and Exercise Metabolism, 24, 127-138.
  4. Layman, D.K.(2009). Dietary Guidelines should reflect new understandings about adult protein needs. Nutrition & Metabolism, 6(12), Lemon, P. (1998). Effects of exercise on dietary protein requirements. International Journal of Sports Nutrition, 8(4), 426-447.
  5. Lucas, M, & Heiss C.J.(2005) Protein needs of older adults engaged in resistance training: A review. Journal of Aging and Physical Activity, 13(2), 223-236.
  6. Moran, L.J., Luscombe-Marsh, N.D., Noakes, M., Wittert, G.A., Keogh, J.B., & Clifton, P.M. (2005). The Satiating Effect of Dietary Protein Is Unrelated to Postprandial Ghrelin. The Journal of Clinical Endocrinology & Metabolsim, 90(9).
  7. Poppitt, S.D., McCormack, D., & Buffenstein, R. (1998).Short-term effects of macronutrient preloads on appetite and energy intake in lean women. Physiology & Behavior, 64(3), 279-285.
  8. Weigle, D.S., Breen, P.A., Matthys, C.C., Callahan, H.S., Meeuws, K.E., Burden, V.R., & Purnell, J.Q. (2005). A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. The American Journal of Clinical Nutrition, 82(1), 41-48.
  9. Westerterp, K.R. (2004). Diet induced thermogenesis. Nutrition & Metabolism, 1, 1-5

What Enzymes Does Mercury Inhibit?

Mercury is a heavy metal that has been used for centuries as a medicine and a poison. Common exposures come from contaminated seafood, dental amalgams, and vaccines for infants. Mercury can exist in 11 different chemical states or compounds. At the molecular level, it forms bonds with sulfhydryl groups on an enzyme, which are parts of the enzyme that contain a sulfur atom that is attached to a hydrogen atom (SH). Binding of mercury can change the shape of the enzyme and block its activity. Enzymes inhibited by mercury include acetylcholinesterase, catalase, dipeptyl peptidase (CD26), amylase, lipase, lactase and glucose-6-phosphatase.

Acetylcholinesterase

Acetylcholine is one of the main neurotransmitters that nerves use to control muscle movement. After release, acetylcholine must be degraded in order to stop the “go” signal from continuing to stimulate the receiving cell. Acetylcholine is degraded by an enzyme called acetylcholinesterase. This enzyme is found in the synaptic cleft, which is the space between the "fingertips" of a nerve cell and the neighboring cell that the nerve activates. Mercury inhibits this enzyme differently in different species, depending on whether it can easily find a sulfhydryl group to latch onto. For human acetylcholinesterase, it takes millimolar amounts of mercuric chloride (HgCl2) to inhibit the enzyme.

Catalase

Catalase is an enzyme that converts hydrogen peroxide into water and oxygen. Hydrogen peroxide is regularly produced by cells as they make energy in a process called cellular respiration. Hydrogen peroxide is toxic at high levels, so cells get rid of it via the enzyme catalase. Though it is widely known that mercury inhibits catalase, it may do so by binding to sites other than sulfhydryl groups. It is interesting to note that when a person absorbs elemental mercury, which causes brain damage, catalase is the enzyme in the red blood cells that converts elemental mercury into an ionic form (mercuric salt).

Creatine Kinase

Mercury also inhibits the enzyme found in skeletal muscle called creatine kinase. Muscle cells contract by using an energy molecule called adenosine triphosphate (ATP), a molecule with three -- thus the “tri” prefix -- phosphates. Energy is released for an enzyme when the enzyme grabs ATP and breaks off one phosphate, resulting in adenosine diphosphate (ADP) -- “di” means two. A quick way of making ATP is to take a phosphate from a sugar molecule called phosphocreatine and add it to ADP. Creatine kinase is the enzyme that recharges ADP into ATP in this way. Mercury inhibits creatine kinase in several ways. Mercury blocks creatine kinase’s ability to bind ADP or the magnesium ion that the enzyme needs in order to function properly.

Digestive Enzymes

Mercury binds to sulfhydryl groups, which is found on the amino acid cysteine. Since cysteine is a common amino acid in many enzymes, mercury inhibits a whole host of enzymes. The "Journal of Applied Toxicology" reported the effects of inorganic mercury in the liver tissue of freshwater fish. Mercury inhibited many enzymes involved in digestion of food molecules, such as protein, carbohydrate and fat: amylase, lipase, lactase and maltase. Mercury also inhibited glucose-6-phosphatase, an enzyme involved in the production and export of glucose in cells.

A Heads-Up Look at Brain Health

Medical advances of today and the very near future — gene therapies, nanotechnology, targeted monoclonal antibodies, cloning, and more — will allow us to “repair” or “replace” damaged and diseased body parts and raise the average life expectancy to 100 years or more. The problem with this magnificent advancement is the studies which suggest that 40% of those reaching 85, and nearly 100% of those reaching 120, will be senile. Of what use is living to a ripe old age if we cannot enjoy it, or even be aware that we’re alive?

Brain Studies

Some 2000 years ago the ancient Greeks attributed all behavior to four temperaments: Hot, Dry, Moist, and Cold. The Romans attributed all symptoms and behaviors to four body fluids, which they called humors: Phlegm, Yellow Bile, Black Bile, and Blood. While Hippocrates, Galen, and hundreds of others slowly advanced the understanding of human anatomy and physiology, the brain sat unstudied for over 1500 years. It was not until the 18th and 19th centuries that brain anatomical science progressed to the point that four distinct lobes were identified, with specific behaviors and body functions ascribed to each.

Over the next 100 years, biochemical and pharmaceutical researchers discovered four separate brain chemicals, called neurotransmitters, that were used by the brain. Somewhat later, four distinct brain waves, or patterns of electrical activity, were discovered and correlated with specific lobes in the brain. Only fairly recently have researchers started to understand this most mysterious organ.

From the 1950s to present, psychiatrists and phychologists have described four broad classifications of human behavior: extroverted or introverted, intuitive or sensing, thinking or feeling, and perceiving or judging. If you suspect that these four primary behaviors can be assigned to a specific lobe, you’d be right!

Brain malfunctions, as manifested by psychiatric problems or unacceptable behavior, can be largely attributed to an imbalance of neurotransmitters within the brain. Unfortunately, discovering these levels within a living brain was not an easy task. (If you think a spinal tap is a risky procedure, just imagine a “brain tap” gone wrong!) What was needed was a simple, noninvasive test to measure the levels of neurotransmitters in a functioning human brain. Various scans of the brain can be employed, but they cannot show actual brain function. For example, an MRI of a patient’s brain right before death and right after death would be identical.

After 25 years of painstaking work, neurological researchers have finally uncovered a long-hidden piece of the puzzle — the relationship between the brain’s chemicals and the brain’s electricity. This discovery allowed clinicians to diagnose brain dysfunction with a simple, noninvasive assessment of the brain’s electrical activity. By measuring the four electrical components of brain activity, doctors can determine the levels of the four neurotransmitters and initiate treatment protocols to correct a deficiency of one or more of them.

Correlation Times Four

Four temperaments; four humors; four neurotransmitters; four lobes; four classes of human behavior; four brain waves; four electrical measurements of brain function. How do these relate? The following table shows the relationship between brain lobes, neurotransmitters, behaviors or personality types, and electrical measurements.

The table above shows the electrical measurements used to determine neurotransmitter levels. As a person ages, his brain goes through a slow decline, or “electropause,” in which the voltage, speed, rhythm, and synchrony change. By measuring these four electrical characteristics, a person’s “brain age” can be determined, which may be younger or older than typical for his chronological age. More importantly, a deficiency in one or more neurotransmitters can be detected and steps taken to restore normal levels.

A computerized diagnostic device called a Brain Electrical Activity Map (BEAM) measures these four values and creates a “picture” of the brain’s electrical activity. It records and tracks the progression of the positive wave created in the brain by an external stimulus, such as a sound (auditory evoked potential) or a flash of light (visual evoked potential).

Speed. A “normal” brain takes about 300 msec (milliseconds) plus a person’s age in years to “think.” This is the measurement of the time delay, or latency, between a stimulus given and the recognition of that stimulus in the brain. As the latency increases (speed decreases), a person moves from mild cognition deficits to severe dementia.

Voltage. A “normal” brain creates an electrical potential of about 10 µv (microvolts). The voltage generated in a person’s brain is related to his ability to concentrate, and low voltage can result in memory impairment, obesity, addictions, or schizophrenia.

Rhythm refers to the regularity of a person’s brain waves. Like cardiac rhythm, the more smooth the rhythm, the better. Brain-wave arrhythmias yield a spectrum of disorders from anxiety and recurring headaches to manic depression and seizures.

Synchrony is a comparison of the electrical activity in each of the hemispheres of the brain. It is common for a person to be dominant in one hemisphere or the other, but a severe imbalance in the electrical activity of the right vs. left hemisphere can lead to sleep disorders, IBS, somatization disorders, or phobias.

Acetylcholine

Review: A “normal” brain takes about 300 msec (milliseconds) plus a person’s age in years to “think.” This is the measurement of the time delay, or latency, between a stimulus given and the recognition of that stimulus in the brain. As the latency increases (speed decreases), a person moves from mild cognition deficits to severe dementia.

Acetylcholine-associated disease states

A diagnostic evaluation of a person’s brain speed can give objective evidence of disturbances in cognition, memory, attention, and behavior. After subtracting the patient’s age, the baseline latency measurement indicates the following: 300 msec is “normal”; 350 msec indicates mild to moderate disturbances in cognitive function (“muddled thinking”); 360 to 370 msec indicates ADD or variability of attention, errors of omission or commission, and delayed reaction time; 380 msec is typically found in Parkinson patients; 420 msec is the threshold for Alzheimer disease, with increasing latency as the dementia progresses. Early detection of deficiencies in the speed at which the brain operates can allow early intervention to slow or reverse the decline, possibly delaying or preventing the onset of Alzheimer and other dementias.

Beyond detecting a frank disease state associated with severe acetylcholine deficiency, physicians can analyze thebalance of the four neurotransmitters to determine a patient’s personality type.

The acetylcholine-dominant personality

Acetylcholine is produced in the parietal lobes, which are responsible for thinking functions such as language processing, intelligence, and attention. People with an excess of acetylcholine (about 17% of the world’s population) are adept at working with their senses and view the world in sensory terms. They are quick thinkers, highly creative, and open to new ideas. Flexibility, creativity, and impulsivity open them up to trying almost anything, as long as it offers the promise of excitement and something new; they are not afraid of failure. They love to travel and have a quest for lifelong learning. These people also tend to be extremely sociable, even charismatic. They love making new friends and put a lot of energy into all of their relationships, whether at work, at home, or in the community. They are eternally optimistic, romantic with their significant other, and attentive to the needs of their children. They are quite popular with a broad range of people. People with extremely high levels of acetylcholine, however, risk giving too much of themselves to others, even to the point of being masochistic. They may feel that the world is taking advantage of them, or they may become paranoid. Too much acetylcholine can drive a person into isolation.

The acetylcholine-deficient personality

Low levels of acetylcholine result when either the brain burns too much or produces too little. Shifts in personality occur at a much milder deficiency than the dementia- producing deficiencies mentioned earlier. These personality traits can, in fact, manifest when the acetylcholine level is only slightly lower than the levels of the other three neurotransmitters. And remember, we’re looking at the relative balance of neurotransmitters. A deficiency in one neurotransmitter is usually offset by an excess of another, which typically produces the personality traits associated with a dominance of that other neurotransmitter.

The eccentric. The absence of thought connections to other people and the world makes this person’s behavior seem odd. The eccentric usually steers away from human interaction and keeps himself isolated. Outwardly, he appears bland and inexpressive. When even mildly stressed, however, he can become a danger to himself and others.

The perfectionist. This person is usually hard working, detail oriented, devoted, and exacting. Self-discipline is a hallmark of this personality type, which can be either a plus or a minus, depending on the severity of the imbalance and which other neurotransmitter is dominant. This person can be an excellent worker, or he can be rigid and obsessive to the point that nothing is actually accomplished. The perfectionist’s life is usually lacking in enjoyment, relaxation, and warmth, which can make that person unapproachable.

Dopamine

Review: A “normal” brain creates an electrical potential of about 10 µv (microvolts). The voltage generated in a person’s brain is related to his ability to concentrate, and low voltage can result in memory impairment, obesity, addictions, or schizophrenia.

Dopamine-associated disease states

A person’s ability to concentrate can be directly correlated with his dopamine level. A diagnostic evaluation of the voltage in a person’s brain can give objective evidence of disturbances in concentration and memory. Low dopamine levels can be involved in difficulty performing routine tasks, a variety of sexual disorders such as loss of libido or anorgasmy, various addictions, from caffeine to opiates, and decreased physical activity due to fatigue. Obesity is a common result of the combination of sugar cravings and low physical activity associated with suboptimal dopamine levels in the brain.

Brain voltage can vary within the range of 0 µv (dead) to 20 µv (super concentration), with 10 µv being classified as “normal.” The voltage range correlates as follows: 0-2 µv is typically found in cocaine babies; 2-4 µv can indicate severe addictions, severe attention deficit disorder, or schizophrenia; 5-6 µv indicates a chronic brain disorder; 7 µv is found in those with moderate addictive behavior, such as caffeine and sugar cravings; 8-9 µv is typical for mild to moderate memory and thinking disturbances, including mild attention deficit; 10 µv is “normal”; and above 10 µv indicates an increased ability to concentrate, even to the rejection of external stimuli at the high end of the range.

Drugs that increase dopamine levels have been used as adjunctive therapy for schizophrenia and opiate addiction. Beyond detecting and treating frank disease states associated with a severe dopamine deficiency, physicians can analyze the balance of the four neurotransmitters to determine a patient’s personality type.

The dopamine-dominant personality

Dopamine is the source of the brain’s power and energy. People with an excess of dopamine (about 17% of the world’s population) thrive on energy. They are likely to be strong-willed individuals who know what they want and how to get it. They are highly rational, more comfortable with facts and figures than feelings and emotions. They can be self-critical, but do not accept criticism or negative feedback from others. These people function well under stress, focusing intently on the task at hand. They are tireless and typically need less sleep than average. Strategeic thinking, invention, and problem-solving are the hallmarks of these individuals. In their personal lives, they like activities related to knowledge and intellect. They can be competitive in sports, but prefer individualized sports over group sports. They tend to establish personal relationships easily, but may have trouble nurturing them. As highly rational people, they have trouble understanding that many people believe feelings are more important than reason. They have a tendency to want to exert control over their spouse and children, and a successful marriage depends on the loyalty and goodwill of the spouse.

People with extremely high levels of dopamine, however, can be overly intense, driven, and impulsive. They may turn to violence as a way of creating controlled environments of excitement and power. Teens may be driven to shoplifting, street racing, or date rape. Criminals — especially repeat sexual offenders — often have extreme dopamine levels and a heightened libido that frequently accompanies it.

The dopamine-deficient personality

Low levels of dopamine result when either the brain burns too much or produces too little. Shifts in personality occur at a much milder deficiency than the disease- producing deficiencies mentioned earlier. Personality shifts can, in fact, manifest when the dopamine level is only slightly lower than the levels of the other three neurotransmitters. And remember, we’re looking at the relative balance of neurotransmitters. A deficiency in one is usually offset by an excess of another, which typically produces the personality traits associated with a dominance of that other neurotransmitter.

Dopamine production determines the brain’s power, as measured by voltage. As the voltage becomes suboptimal, the person literally slows down, mentally and physically. Minor deficiencies can produce a range of mental and physical symptoms, such as mild memory loss, mild depression (“the blues”), panic disorder, PMS, insomnia, fatigue, mild hypertension, nicotine addiction, and obesity. Sexual side effects, such as loss of libido and difficulty achieving orgasm, are common among people with a dopamine deficiency.

The previous two neurotransmitters — acetylcholine and dopamine — can be thought of as the brain’s “on” switch, providing energy, power, and speed. The next two — gamma-aminobutyric acid (GABA) and serotonin — function as the brain’s “off” switch, providing calmness, rest, and sleep. A balance of the “on” and “off” neurotransmitters is necessary for proper brain function.

GABA

Review: Rhythm refers to the regularity of a person’s brain waves. Like cardiac rhythm, the more smooth the rhythm, the better. Brain-wave arrhythmias, or dysrhythmias, yield a spectrum of disorders from anxiety and recurring headaches to manic depression and seizures.

GABA-associated disease states

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain. It has a calming, stabilizing effect. It controls the brain’s rhythm, which allows a person to function at a steady pace and prevent him from becoming too “hyper.” As the brain’s GABA level declines, brain waves begin to become less rhythmic. This can bring on a multitude of symptoms, both psychological and physical.

Mild brain-wave dysrhythmias can produce anxiety and its accompanying physical manifestations: restlessness, sweating, cold or clammy hands, butterflies in the stomach, and a lump in the throat. Other physical symptoms that can appear with a moderate GABA deficiency include carbohydrate cravings, an abnormal sense of smell, and unusual allergies. As GABA levels further decrease, anxiety can become more pronounced and produce attention-deficit disorders, PMS, flushing, trembling, hypertension, cystitis, and gastrointestinal disorders. At the most extreme deficiency, this can become full-blown panic attacks, manic depression, migraine headaches, hyperventilation, palpitations, tachycardia, blurred vision, tinnitus, twitching, and seizures. Advanced psychological symptoms can include severe delusions, feelings of dread, and a short temper that can progress into full-blown rage reactions and violence. Chronic marijuana and alcohol abuse can signal an acute GABA deficiency.

Beyond detecting and treating frank disease states associated with GABA deficiencies, physicians can analyze thebalance of the four neurotransmitters to determine a patient’s personality type.

The GABA-dominant personality

People with high GABA levels (about 50% of the world’s population) share the common attributes of stability, consistency, sociability, and concern for others. They are nature’s most dependable people. They can be counted on to show up at work every day and be there when others need them. At work, GABA- dominant people are the ones who set goals, organize projects, schedule activities, and keep others on task. Their punctuality, objectivity, practicality, and confidence make them excellent employees. Organization is paramount to them — at work, at home, and in their social life. It’s no wonder that these people gravitate to careers as administrators, accountants, air-traffic controllers, meeting planners, nurses, EMTs, and yes, medical transcriptionists. They’re the ones in the group who stay focused on the matter at hand. They are the consummate team player, both metaphorically and literally. In their personal life, such people derive pleasure from taking care of their family and friends. They can be a serene island in a sea of chaos. Although they like group activities, they cherish one- on- one relationships. Their friends are forever, and their marriage is a long- term commitment. Nurturing and making others happy is their ultimate goal. They tend to be religious and believe in traditions, especially where friends and family are involved, such as holiday gatherings.

As with the other neurotransmitters, it is possible to have too much of a good thing. People who produce too much GABA can be organizational to the point of setting rigid schedules and micromanaging others, whether as a boss, a coworker, a friend, or spouse. Excess GABA can dramatically increase a person’s nurturing tendencies. They can spend enormous amounts of time and energy looking for opportunities to give love and care to others, at the cost of their own needs not being met.

The GABA-deficient personality

Low levels of GABA result when either the brain burns too much or produces too little. Shifts in personality occur at a much milder deficiency than the disease- producing deficiencies mentioned earlier. Personality shifts can, in fact, manifest when the GABA level is only slightly lower than the levels of the other three neurotransmitters. And remember, we’re looking at the relative balance of neurotransmitters. A deficiency in one is usually offset by an excess of another, which typically produces the personality traits associated with a dominance of that other neurotransmitter.

Unlike a balanced brain that creates energy in a smooth, steady flow, a person with low GABA creates energy in bursts. This brain dysrhythmia can upset the body in a number of ways, but none is more pronounced than in the realm of emotional well- being. Specifically, he can lose the ability to effectively deal with life’s stresses. He may begin to feel nervous, anxious, and irritable. He may demonstrate poor emotional stability, lack impulse control, and resort to childish behavior. It can also manifest as poor verbal memory and difficulty concentrating. Physically, low GABA levels can bring on a variety of subacute conditions such as allergies, transient aches, instability while walking, diarrhea or constipation, and insomnia or hypersomnia. Usually, such physical annoyances occur one after another to the point that a person begins to wonder about his general state of health.

Serotonin

Review: Synchrony is a comparison of the electrical activity in each of the hemispheres of the brain. It is common for a person to be dominant in one hemisphere or the other, but a severe imbalance in the electrical activity of the right vs. left hemisphere can lead to sleep disorders, IBS, somatization disorders, or phobias.

Serotonin-associated disease states

Correlating with delta waves in the brain, serotonin affects your ability to rest, regenerate, and find serenity. Adequate serotonin allows the brain to recharge and rebalance itself each night, so that you can begin each morning with a fresh start. Serotonin is produced in the occipital lobes, which is also the center of sight.

As serotonin levels drop, the right and left hemispheres become desynchronized, producing feelings of being out of control. Moderately low levels can produce depression, mild hypertension, arthritis, poor temperature regulation, sexual disturbances such as premature ejaculation or delayed arousal response, bowel disturbances, mild PMS with emotional outbursts, learning disorders, obsessive- compulsive behavior, and insomnia, which tends to further lower serotonin levels. As levels drop further, hypertension can become uncontrolled, arthritis can intensify, PMS can become severe, and a wide range of perimenopausal symptoms can occur. With a severe shortage of serotonin, physical and psychological disturbances may become life threatening, with bingeing, masochism, severe depression and other serious mood disorders, addictions including alcoholism and drug abuse, somatization disorders, schizoaffective disorders, and schizophrenia with hallucinations. Physically, a severe serotonin deficiency can cause insomnia/ hypersomnia sleep cycles measured in days and increase hypertension to the point of producing a stroke.

Beyond detecting and treating frank disease states associated with serotonin deficiencies, physicians can analyze the balance of the four neurotransmitters to determine a patient’s personality type.

The serotonin-dominant personality

People with high serotonin levels (about 17% of the world’s population) know how to live in the moment. Realistic and impulsive, they are highly responsive to sensory input. They’re active participants in life who thrive on change. They take their vacations at a different spot each year. They try new foods, new hobbies, and new friends, and they have a natural disdain for order, structure, and authority. They’re optimistic, cheerful, easygoing, and the life of the party. A serotonin-dominant person gravitates to trades or professions that offer a variety of tasks, an ever-changing environment, and interactions with different people. Their keen hand-eye coordination makes them well suited to using various tools to accomplish their tasks. Construction workers, truck drivers, military personnel, hairstylists, pilots, surgeons, chiropractors, movie stars, fashion models, photographers, and professional athletes likely owe their skills to ample serotonin levels. Preferred sports can include mountain climbing, hunting, skydiving, hang gliding, scuba diving — just about anything that offers a personal challenge along with a certain level of excitement. They play hard and have the time of their life when doing activities that others would consider too dangerous. In relationships, they can be romantic and passionate, but they also love their independence and often refuse to be tied down. Due to their impulsivity and desire for change, they tend to move away from people before deep relationships develop. In fact, their friendships are typically many and varied — wide instead of deep. They have a fondness for children, but make better aunts and uncles than parents.

As with the other neurotransmitters, it is possible to have too much. An excess of serotonin can make a person extremely nervous. He can become hesitant, distracted, hypersensitive to criticism, and morbidly afraid of being disliked. Excessive serotonin can make a person believe he is inadequate and inferior. Sadness and anger are constant companions, and although he may have a desperate desire for interpersonal interaction, he is too fearful to even make an attempt.

The serotonin-deficient personality

Serotonin deficiency can occur from experiencing too much excitement (thereby metabolizing large amounts of serotonin) and/or not getting sufficient sleep (causing the brain to generate less serotonin). Shifts in personality occur at a much milder deficiency than the disease- producing deficiencies mentioned earlier. Personality shifts can, in fact, manifest when the serotonin level is only slightly lower than the levels of the other three neurotransmitters. And remember, we’re looking at the relative balance of neurotransmitters. A deficiency in one is usually offset by an excess of another, which typically produces the personality traits associated with a dominance of that other neurotransmitter.

A common sign of serotonin deficiency is depression and fatigue. The chronic lack of sufficient sleep means that the brain is unable to rest, regenerate, and resynchronize. This can manifest in the personality as a flat affect (a classic sign of depression) and a lack of pleasure, artistic appreciation, and common sense. The person may become codependent, obsessive- compulsive, or exhibit loner tendencies. He can be impulsive or perfectionistic, painfully shy or masochistic. Someone with multiple phobias is typically serotonin deficient. The frequent use of ecstasy, PCP, and LSD also signals a serotonin deficiency.

Lettin’ the good guys in,
Keepin’ the bad guys out

We have been made with a wonderful mechanism to prevent harmful substances from entering the brain. Not everything that circulates in the blood stream is allowed entry into the brain. There is a barrier between the blood and the brain, logically called the blood-brain barrier, that allows only glucose and certain nutrients selective access to the brain. This membrane protects the brain from toxins and other substances that would cause it damage. It also “holds in” certain substances manufactured by the brain, notably neurotransmitters, that would be lost through diffusion throughout the rest of the body if allowed to pass into the blood stream. Therefore, the same membrane that prevents toxins from passing through also prevents neurotransmitters from passing through. This characteristic of the blood-brain barier is the reason why a Parkinson disease patient, for example, cannot receive an injection of dopamine to restore the dopamine level in his brain and reverse the disease. So the dilemma is how to raise the level of specific neurotransmitters in the brain, when simple supplementation with those neurotransmitters is ineffective.

The answer lies in finding a way to “coax” the brain to produce more endogenous neurotransmitters. It turns out that the answer is fairly simple — give the brain more raw material, and it will make more neurotransmitters. Fortunately, the mechanism by which the brain makes each neurotransmitter is well known. Like most substances in the body, they are made through a series of chemical reactions. Notice that I said the blood-brain barrier allows only glucose and certain nutrients selective access to the brain. It is those “certain nutrients” that the brain uses to make neurotransmitters. If there is a deficiency in any of the nutrients needed to make a specific neurotransmitter, there will be a corresponding deficiency of that neurotransmitter. Supplementing the deficient nutrient(s) will allow the brain to resume full production of the neurotransmitter.

Building a better brain

So what are the “certain nutrients” that the brain must have? Without going into the chemistry of neurotransmitter manufacture, suffice it to say that the brain’s supply of amino acids is the most common limiting step in their production. Amino acids, the basic building blocks of protein, are also the basic raw material the brain uses to function. As such, they easily cross the blood-brain barrier. All amino acids can cross the blood-brain barrrier, in fact, but not all are used to make neurotransmitters. The problem is that all the amino acids circulating in the blood stream at any given time compete for passage through the “amino acid channels” in the blood-brain barrier, and passage of a specific amino acid is granted in proportion to its concentration in the blood. If you eat a steak or other complete protein source, all 20 amino acids are simultaneously competing for entry into the brain. Supplementing with, say, 1 gram of a certain amino acid won’t do much if you chase it with a glass of milk (15 grams of protein in 12 oz.) or take it with a meal. To be effective, amino acid supplements should be taken on an empty stomach with plain water or fruit juice (the fructose in juice helps escort the amino acid to the brain).

In the paragraphs that follow, I will tell you which amino acids are used to boost which neurotransmitter, and the primary food sources for that amino acid. Food sources are complex, however, and foods that boost the production of one neurotransmitter can also contain substances that boost the production of another. Eggs, for example, provide a tremenous boost for acetylcholine, but they also have a component that supports GABA. This is one reason why a change of diet takes longer to produce an effect than supplementation with pure amino acids. You should know that prescription drugs are also available to boost the production of a specific neurotransmitter or slow its destruction, but that is beyond the scope of this article. They are listed in detail in the reference given at the end of the article. (Note: numbers shown after the supplements listed below refer to the relative efficacy in boosting the neurotransmitter, on a scale of [1]=best to [4]=least effective.)

Boosting acetylcholine

  • Pure amino acid precursors: serine, carnitine.
  • Amino acid-boosting supplements: DMAE (dimethylaminoethanol) [1], phosphatidylcholine [1], phosphatidylserine [2], acetyl-L-carnitine [2], GPC (glycerol phosphocholine) [3].
  • Supporting supplements: huperzine A [1], nicotine [1], lipoic acid (alpha-lipoic acid) [3], fish oils [3], manganese [4], conjugated linoleic acid [4].
  • Hormonal supplements: DHEA (dehydroepiandrosterone) [2].
  • Illegal supplements: LSD, PCP, psychotropic mushrooms.
  • Dietary support: choline-rich foods, including avocado, cucumber, zucchini, lettuce, most fruit, bacon, bologna, hot dogs, chicken, turkey, pork, liver, fish, beef, milk, ice cream, sour cream, yogurt, cheese, eggs, and various nuts.
  • Lifestyle support: aerobic exercise.

Boosting dopamine

  • Pure amino acid precursors: phenylalanine, tyrosine.
  • Amino acid-boosting supplements: N-acetyl tyrosine [2], L-tyrosine [3], phenylalanine [3]. (Note: most ingested phenylalanine is hydroxylated to tyrosine in the body. Tyrosine supplements, therefore, need one less chemical conversion step to be used by the body.)
  • Supporting supplements: caffeine [1], guarana [1], yohimbe [1], ephedra[2], nicotine [2], Rhodiola rosea[3], thiamine [4], chromium [4], folic acid [4].
  • Hormonal supplements: DHEA [2].
  • Illegal supplements: cocaine, ecstasy, mescaline.
  • Dietary support: phenylalanine- and tyrosine-rich foods, including wild game, duck, turkey, pork, chicken, luncheon meats, cottage cheese, ricotta, milk, yogurt, walnuts, soybeans, wheat germ, granola, rolled oats, dark chocolate, and eggs.
  • Lifestyle support: sexual activity (for women), weight-bearing exercise, aerobic exercise.

Boosting GABA

  • Pure amino acid precursor: glutamine.
  • Amino acid-boosting supplements: L-glutamine [1].
  • Supporting supplements: inositol [1], alcohol [1], B vitamins [2], glycine [3], kava [3], BCAA (branched-chain amino acids) [4], taurine [4].
  • Hormonal supplements: progesterone [2].
  • Illegal supplements: opioids, ketamine, marijuana, quaaludes.
  • Dietary support: glutamine-rich foods (especially complex carbohydrates), including almonds, walnuts, and other tree nuts, whole-grain wheat and oats, rice bran, brown rice, lentils, potatoes, broccoli, spinach, bananas, citrus fruit, halibut, and beef liver.
  • Lifestyle support: sexual activity (for men and women), sleep, aerobic exercise.

Boosting serotonin

  • Pure amino acid precursor: tryptophan.
  • Amino acid-boosting supplements: L-tryptophan [2], 5-HTP (5-hydroxytryptophan) [3].
  • Supporting supplements: St. John’s wort [2], vitamin B6 [4], fish oils [4].
  • Hormonal supplements: melatonin [1], progesterone [2].
  • Illegal supplements: LSD, PCP, GHB, ecstasy.
  • Dietary support: tryptophan-rich foods, including wild game, pork, luncheon meats, duck, turkey, chicken, wheat germ, cottage cheese, and eggs.
  • Lifestyle support: aerobic exercise, psychotherapy, sleep.

To learn more

This series of articles is a synopsis of the groundbreaking research of Eric R. Braverman, MD, as presented at the American Academy of Anti-Aging Medicine (A4M) Annual Conference, June 2003. Dr. Braverman was a member of the pioneering research team at Havard University that developed the BEAM (Brain Electrical Activity Map), a noninvasive device to measure neurotransmitter levels in functioning brains through electrical activity. For more information, his book, The Edge Effect, is highly recommended reading.

The Importance of Zinc

The human body absorbs approximately 400kg zinc over the average 70-year lifespan and at any one time there should be 2-4 gm zinc in the body. It is the second most abundant mineral ion ( Magnesium is the first) in the body and is the only metal that appears in all enzyme classes The body absorbs 20-40% of zinc in food, zinc from animal foods being more readily absorbed (twice as much ) than zinc from plant foods. Zinc is also more readily absorbed with a protein meal and although the body cannot store zinc and it is needed every day in small amounts (50mg or less), it may be held in metallothionine reserves and transferred in metal transporter proteins. Metallothionines in the intestinal cells are capable of adjusting the absorption of zinc by 15-40%. Thus control of cellular zinc homeostasis is maintained by zinc proteins and zinc binding metallothioneines. Zinc is needed for over 300 enzymes in the body and makes up part of 3000 different proteins in the body. Muscles (60%) and bones (30%) contain 90% of the body’s zinc. High concentrations of zinc are found in the prostate gland and semen and the choroid of the eye.

If bone is reabsorbed or muscle is broken down then some zinc can be reutilised and in cases of zinc depletion changes in immune status alter before any decrease in levels of plasma zinc. There is a small exchangeable pool of zinc (100-200mg ) that depends on recently absorbed zinc and the intestinal excretion of zinc. As with Magnesium, the efficiency of absorption of zinc is inversely related to the amount of zinc present in the body. The greater the level of body zinc, the less absorption occurs. Zinc, Magnesium Calcium and Iron all compete for transporters in the intestine for uptake above a threshold of approximately 800mg so consuming these minerals together below this level should not interfere with uptake Zinc is found in all cells in the body and the daily requirement is dependent on age and activity.

Zinc deficiency is due to

  • Soil deficiency.

  • Some drugs deplete zinc.

  • Vegetarian and vegan diets may be deficient.

  • High cereal based diets, containing high phytate foods which can bind with zinc and impair absorption.

  • Cooking with water can result in leaching of up to 50% of zinc levels of the food.

  • Refined processing of wheat and baked goods can result in up to 75% zinc loss

 

Tetracycline and quinolone antibiotics react with zinc in the intestines inhibiting the absorption of both the antibiotic and zinc. The antibiotic should be taken 2 hours or more before or at least 4-6 hours after the zinc supplement to avoid this. 

In short over 300 enzymes are zinc dependent, including enzymes involved in the synthesis of certain proteins such as collagen and wound healing. Also needed for thymic hormone activation and maintaining a normal immune system, testosterone and oestrogen, fertility and reproduction including cell division. It is involved in gene regulation, maintaining acid/base balance in the body and normal carbohydrate, fat and protein metabolism. It is needed for normal bones, skin, hair and nails and normal brain function including maintenance of normal vision. It can also act as an antioxidant, protecting DNA, lipids and proteins in the body.

Zinc Contributes to

Normal DNA synthesis. Although the exact role of zinc in DNA synthesis is not fully understood but it does play a structural role in zinc fingers, which are finger shaped proteins. Due to their shape, these proteins can bind to DNA and RNA allowing them to function in Gene expression. These proteins are the most common transcription factors in living organisms, transcription factors are proteins that bind to DNA and control the transfer of genetic information to RNA Put simply Zinc is needed for reading genetic instructions and lack of zinc may mean that instructions get misread or not read at all.

Normal acid/base metabolism. Acid/Base balance is the balance between acid and alkaline to keep body fluids as close to a neutral pH (pH7) as possible. Carbon dioxide and water are rapidly converted to bicarbonate and water (and back again) to maintain acid base balance in the blood and other tissues. The enzyme responsible for this is the zinc dependent enzyme Carbonic Anhydrase. Studies have shown that dietary deficiency of zinc reduces red blood cell carbonic anhydrase activity

Normal carbohydrate metabolism. Deficiency of zinc results in a drop of metabolic rate. Zinc dependent messenger RNA is needed to synthesise the enzymes required for carbohydrate metabolism so zinc deficiency may result in lack of these enzymes. Zinc may also interact with insulin by controlling the uptake of glucose by adipocytes (fat cells). Zinc deficiency results in impaired carbohydrate metabolism.

Normal cognitive function Zinc is highly concentrated in the cerebral cortex, pineal gland and hippocampus and zinc deficiency is associated with impaired memory formation and mood disorders. In the hippocampus zinc can reach concentrations of 8% of the total brain zinc. Zinc ions are also NDMA (N-methyl-D –aspartate) antagonists (NDMAs control memory function and excessive NDMA activation results in cell death due to excess calcium influx into neuronal cells ) so zinc becomes important for normal neuronal function and memory and delaying brain cell death . Normal fertility and reproduction. Steroid hormones such as testosterone and oestrogen are derived from cholesterol and zinc plays an important role in cholesterol metabolism. Low dietary zinc is associated with low concentrations of several hormones including testosterone.

Testosterone. Circulating testosterone and free testosterone appears to increase with oral zinc intake. In one study supplementing with 250 mg zinc sulphate for 6 weeks increased testosterone by 85% in people on hemodialysis.

Free Testosterone is converted to DHT (dehydrotestosterone) by the enzyme 5alpha-reductase ) primarily in the prostate gland, testes , adrenal glands and hair follicles. DHT is increased in infertile men and as it has an affinity for the hair follicles can result in male pattern baldness. Zinc has been shown to inhibit ( up to 98%)the enzyme 5 alpha reductase.

Semen: Semen is very rich in zinc. Sperm count, motility and physical characteristics of sperm increase and improve with some groups of infertile men.

Zinc deficiency has also been associated with increased expression of oestrogen receptors. The enzyme aromatase converts testosterone to oestrogen and zinc decreases aromatase activity so preventing excessive conversion of testosterone to oestrogen. Zinc deficiency can cause testicular cell death, increase protein oxidation in the testes, dysregulating other enzymes and proteins resulting in degeneration of testicular structures and impaired testosterone secretion.

Why should I Take A Zinc Supplement?

Normal macronutrient metabolism. Macronutrients are carbohydrates, fats and proteins. Zinc is needed for the enzymes that metabolise carbohydrates, fats and proteins

Normal metabolism of fatty acids- zinc is needed for the conversion of linoleic acid to Gamma Linolenic acid (GLA) and for the synthesis of prostaglandins series 1 ( Anti inflammatory prostaglandins) Zinc also plays an essential role in maintaining a balance between to different forms of prostaglandins.

Maintenance of normal serum testosterone concentrations, so involved in fertility and reproduction. Zinc plays a role in cell signalling, influencing hormone release and nerve function.

Normal metabolism of vitamin A. Zinc is necessary to maintain normal concentrations of vitamin A in the plasma, being essential for normal mobilization of Vitamin A from the liver. Zinc deficiency decreases the synthesis of Retinol Binding protein (RBP) in the liver leading to lower levels of RBP in the plasma.It influences the absorption, transport and utilisation of Vitamin A. . Zinc is also required for the enzyme Alcohol dehydrogenase , responsible for converting retinol to retinal, essential for eye function.

Normal protein synthesis. One of the important zinc dependent proteins is Gustin which is involved in taste and smell. Poor or absent gustin levels results in impaired taste and smell. Other important zinc containing enzymes are carboxopeptidase which helps break down protein. Zinc deficiency also impairs the synthesis of the protein Opsin, the precursor of Rhodopsin, which if decreased, results in abnormal dark adaptation of the eye. Zinc is also required for the enzyme alcohol dehydrogenase , responsible for converting retinol to retinal, essential for eye function. Haemoglobin is a protein and zinc s important in haemoglobin synthesis.

Maintenance of normal bones. Zinc regulates the secretion of calcitonin from the thyroid gland and therefore influences bone turnover. Zinc appears to regulate the bone matrix calcification in osteoblasts. Zinc deficiency decreases the activity of matrix proteins, type 1 collagen and alkaline phosphatase decreasing Calcium and Phosphorus accumulation. Therefore zinc deficiency may become a risk factor for poor extra cellular matrix calcification.

Maintenance of normal hair and nails Zinc is needed for building keratin and formation of collagen and for facilitating cell division that makes hair growth possible.

Maintainance of normal skin. Collagen in skin is produced by zinc dependent enzymes , the collagenases. Type 1 collagen is produced in the skin and is a structural long lived protein produced by fibroblasts. Collagen constitutes 70% skin mass and give the skin its structure and resistance to traction and strains. Total collagen decreases 1% a year resulting in decreased elasticity and aging skin. Zinc is essential not only for the enzymes producing collagen but also the cross linking that give collagen its stability. Human studies have shown that decreased zinc resulted in decreased total collagen.

Maintenance of normal vision Zinc supplementation alone significantly reduced the risks of developing AMD in subjects at higher risk. Zinc deficiency also impairs the synthesis of the protein Opsin, the precursor of Rhodopsin, which if decreased, results in abnormal dark adaptation of the eye. Zinc is also required for the enzyme alcohol dehydrogenase , responsible for converting retinol to retinal, essential for eye function.

Contributes to normal function of the immune system. Plays a central role in the immune system affecting cellular and humoral immunity. It is essential for thymic dependent T cells . Zinc deficiency results in decreased levels of all types of white blood cells. It is also required for the production of Thymulin (thymic hormone) Zinc ions also exhibit direct anti microbial activity.

Contributes to protecting the cells from oxidative damage, protecting the DNA, lipids and proteins . Loss of zinc from biological membranes increases their susceptibility to oxidative damage. Zinc is also necessary for the antioxidant enzyme Super Oxide Dismutase (SOD)and low levels of zinc supplementation resulted in increased levels of glutathione peroxidase , SOD and decreased lipid peroxidation.

The process of cell division. Zinc contributes to normal DNA synthesis and cell division. Zinc appears to be essential for Insulin like growth factor (IGF) which induces cell proliferation. Reduced zinc availability appears to affect membrane signalling and secondary messengers that coordinate cell proliferation. Ref : The Role of Zinc in Growth and Cell Proliferation by Ruth MacDonald published In The American Society for Nutritional Sciences Reference

What Are The Symptoms Of A Mild Zinc Deficiency?

  • Loss of appetite.

  • Poor growth.

  • Weight loss.

  • Diminished taste or smell.

  • Poor wound healing.

  • Skin problems, acne, psoriasis atopic dermatitis.

  • Poor vision, night blindness.

  • White spots on finger nails.

  • Depression, apathy.

What Are The Symptoms Of A Severe Zinc Deficiency?

  • Delayed sexual and bone maturation

  • Skin lesions

  • Diarrhoea

  • Loss of appetite

  • Hair loss

  • Increased susceptibility to infections

  • Behavioural changes

The passage of zinc into the body

Studies involving direct comparison of bioavailability of different forms of zinc in humans are few. The important fact is that the form of zinc needs to become dissociated into zinc ions which then bind to ligands ( proteins ) that transport the zinc into the cells of the small intestine. There are specific transport proteins that carry zinc across the cell membrane into the portal circulation where it is transported directly to the liver before being released into the circulation for delivery to all tissues. Approximately 70% of zinc is bound to serum albumin ( a plasma protein ) and factors altering serum albumin in turn affect serum zinc levels. Serum zinc has a rapid turnover to meet tissue demands.

Zinc is lost through the skin and kidneys (combined loss of 0.5-0.8mg/day) , more zinc being lost when the body sweats more, as in hot climates and during strenuous exercise. Approximately half of all zinc eliminated from the body is lost through the shedding of epithelial cells in the gastro intestinal tract (0.5- 3mg/day) and although a considerable amount is secreted through both biliary and intestinal secretions, most of the secretions are reabsorbed regulating the zinc balance. Starvation and muscle breakdown also increase zinc loss through the urine.

As already mentioned, protein enhances the absorption of zinc and a phytate rich diet (from cereals, grains, corn and rice) inhibit the absorption of zinc.

There is a very fine balance between zinc and copper. Zinc reduces the amount of copper your body absorbs because copper competes with zinc to bind with metallothionein, the binding protein that brings zinc into the intestinal cells. The ratio of zinc : copper is arguably more important than the concentration of either copper or zinc, a common problem being excessive copper in water from copper pipes or copper cookware.

Zinc also competes with iron to bind with blood transferring, illustrating the importance of a balance of these minerals. The ECRDA for zinc is 10 mg less is required for babies, children and teenagers and more for pregnant and breastfeeding ladies.

Recommended Daily Allowance For Zinc Supplements

Bioavailability Of Different Forms Of Zinc Supplements

There are many forms of zinc compounds. 

  • Zinc Picolinate 20%

  • Zinc Ascorbate 15%

  • Zinc Chloride 48%

  • Zinc Sulphate 22%

  • Zinc Carbonate 52%

  • Zinc Citrate 31%

  • Zinc Bisglycinate 25%

There is not much substantial evidence of greater effectivity of one form of zinc over another as absorption of zinc in the body is subject to so many variables.

However, a small research study (15 healthy young adults in a randomised, double blind three way cross over study, receiving 10mg of elemental zinc as a supplement without food just published (20 November 2013) found that the bioavailability of zinc citrate was 61.3% , of zinc gluconate was 60.9% and of zinc oxide was 49.9 % Previous zinc intake may affect zinc bioavailability studies. Variables include;

  • Existing zinc status of the individual. The lower the zinc status of the individual, the greater the absorption of zinc.

  • People that sweat a lot are subject to more zinc loss, for example athletes, those in hot climate, menopausal ladies experiencing night sweats.

  • Dosage of zinc- as zinc intake in dosages is increased , percentage absorption decreases probably due to the saturation of the transport mechanisms.

  • Zinc absorption appears to be decreased in the elderly.

  • Zinc absorption is increased with dietary protein intake.

  • The type of protein in a meal affects zinc bioavailability. Animal protein enhances absorption.

  • Phytates in cereals and soy inhibit absorption of zinc by binding with it ( except zinc bisglycinate found in Metabolics zinc formula).

  • Caesin in milk and calcium inhibit absorption by binding with zinc ions.

  • Iron inhibits absorption of zinc.

  • Copper ( in high amounts ) inhibits Zinc absorption. In studies using 15mg zinc combined with 2mg copper no inhibition of absorption was found.

  • Cadmium- toxic levels of cadmium can inhibit zinc absorption

Conclusion

Types of zinc supplements may remain a personal preference, although generally zinc should not be taken on an empty stomach (as it can result in nausea) should be taken with an animal protein meal , away from cereals and taken in conservative doses to increase absorption. Long term zinc intake is recommended with copper (see zinc formula) as this is zinc bisglycinate, the only form not affected by phytates and balanced with a small amount of copper.

 

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