I am really surprised that there are so many pictures out in the internet of me over the years. I even recovered a few I had misplaced. The Google Images.

Yesterday I was at the Tropicana for a meeting and the waitresses thought I looked liked Michael Douglas. I told them I was his father, Kirk,  who is 10 or more years older than I and a wonderful example of a life devoted, not to fitness, but to vanity. I fall in that category too. They came back to our table often to look at me, the same way younger males check out my 75-year old WW. It is all fun and not something my WW and I take seriously. But, to tell the truth, we look good and far younger than our ages.

It is far more important to regard your appearance and health as measures of your  success than to claim you are saving the human race or something to that effect. For me, health is mostly about looking good and that turns out to be a very accurate scale. Far more accurate than LDL, BMI, or blood glucose readings.

As I approach my 76-th birthday this August, I have made some changes in how I eat and exercise. I weigh about 203.6 +- 2 pounds and my body fat reading several days in a row is from 5.3 to 5.6%.  That I continue to weigh what I have weighed for the past 50 years while eating a bit less and carrying less body fat than I ever have says something about what I have been doing. My body composition has improved with a bit more muscle and less fat while remaining at the same weight.

I want to share that with you and let you make up your own mind about following this approach or something similar to it. This post is about the diet, eating pattern and supplements I take. The next post will discuss my new way of exercising.

The changes are simple:

• I most often eat just two meals a day, as was the practice in Medieval England and many other places and locations around the world even today. Now and then, I eat three meals.
• I exercise, not counting play as exercise, a bit more; usually 4 times a week. The workouts are usually well less than half an hour, but they are done in new way (next post).
• I have been using Branched Chain Amino Acids far more.

The star of this regimen, if there is one, is the Guardian BCAAs with B12 that I co-developed with Dr. Demopolous. I have only sparingly used BCAAs over the years, but now I am a big fan. They keep me from getting hungry, keep my brain from lacking energy, promote muscle growth, and, above all, protect and stimulate my mitochondria. As you will see below from my references, the BCAAs give my body a metabolic advantage on both sides of the energy equation.

On the energy expenditure side, the BCAAs stimulate energy production through mitochondrial biogenesis and activity, by stimulating muscle growth, by increasing fat leptin secretion, by decreasing body weight via mTOR signaling, and by improving muscle glucose uptake and whole body glucose metabolism. This is at least a triple hit on the energy expenditure side.

On the energy intake side, the BCAAs provide energy substrate for my brain, so I do not get hungry, they decrease food intake and increase insulin sensitivity and improve antioxidant defenses.

I think the central mechanism that drives what we call aging is a shift in protein synthesis and loss toward a net loss of muscle protein. That is to say, the balance of protein degradation (catabolism) and protein addition (anabolism) shifts from growth or maintenance to a loss of body protein. This seems to be the underlying mechanism behind the progression to sarcopenia and loss of strength that is almost universal among the aging. Not only muscle protein is diminished, so is organ and mitochondrial protein, as well as enzymes and neurotransmitters.

As I said in my book, our mitochondria are guests in our cells and have their own agenda. Their fate is tied to the cell in which they reside, which offers them protection and nutrients. Mitochondrial and nuclear DNA were exchanged eons ago, tying their fates together. Thus, we age in direct proportion to the density and function of our mitochondria. These helpful partners can promote the nuclear cell or execute a death program  to kill it.  

I believe I am leaner and more muscular than at any stage of my life because I have focussed on my mitochondria using the tools of autophagy, ICR, and FT-specific exercise along with an increased intake of BCAAs. My approach emphasizes switching between anabolic and catabolic states. It is the switching of anabolic and catabolic states with autophagy intervening that promotes muscle growth and quality by clearing damaged proteins and maintaining the density of mitochondria. That is the focus of my eating and exercise.

To give some idea of the importance of mitochondrial density and function, I qoute from D’Antona et. al cited below that supports ICR, strength exercise, and BCAA supplementation:

“Among the plethora of biological phenomena affected by aging, the malfunction of mitochondria and the decrease of mitochondrial biogenesis, together with increased oxidative damage, seem to exert some of the most deleterious effects on the organism (Guarente, 2008; Lopez-Lluch et al., 2008). A variety of strategies that alleviate age-related deficits in mitochondrial biogenesis and activity, including calorie restriction (CR) and moderate physical exercise, promote survival in mammals. These interventions increase the expression of peroxisome proliferator-activated receptor g coactivator-1a (PGC-1a, a master regulator of mitochondrial biogenesis and reactive oxygen species [ROS] defense system) and of sirtuin 1 (SIRT1, a member of the sirtuin family linked to life span extension, enhanced mitochondrial biogenesis, and decreased ROS production), thus reducing oxidative damage in metabolically active tissues of mice and humans (Civitarese et al., 2007; Nisoli et al., 2005; Ristowet al., 2009)....Here, we demonstrated that the BCAA supplementation increased average life span of male mice, and this was accompanied by increased mitochondrial biogenesis and SIRT1 expression both in cardiac and skeletal muscles, unlike adipose tissues and liver of middle-aged mice. Further, the muscle ROS defense system genes were upregulated by BCAA supplementation, resulting in decreased indices of oxidative damage.”

Here is what I am doing on the eating and supplement side.

• I am eating rather pure, which I prefer to do, but now with real purity. That means no bread or milk, rice, potatoes, or beans and limited fruit. I still trim my meats if I eat beef and am eating more seafood, chicken and pork than beef. I suggest that this eliminates most all sources of inflammation from my diet.
• On most days, I eat just twice a day. I do not eat nuts in the evening as I am sometimes inclined to do. When I feel hungry after a few days at this level, I will eat three times or eat a really large, but early dinner. This is all done by feel with no planning and the eating is spontaneous, not scheduled.
• I work out at least 4 times a week, in very brief workouts that I will describe later. I have long felt that 1, 2, or 3 workouts a week is insufficient to give the muscle quality that I seek.

I take about from 1 to 2 grams of Guardian BCAAs with B12 a day. I use a teaspoon if I am hungry and do not want to stop to eat. I take another mid day for an energy boost, if convenient, and another an hour after dinner and well before bed.  The BCAAs supply for my liver to go into gluconeogenesis to make glucose for my brain’s energy supply. The BCAAs with the B12 encourages my mitochondria to increase in size, function, and number by upregulating protein synthesis in the mitochondria. The B12 has a little known, subtle effect on the electrical coupling of the mitochondria, which I think only Dr. Demopulous understands. We put the B12 in the BCAAs at his suggestion and you can see it as small dark crystals in the BCAAs. In my humble opinion, it is the BCAAs that have brought my fat level down to less than 6% on most scale readings.

I simply do not get tired as a result of these doses of BCAAs with B12. Taking a teaspoon with plain water may be the best energy drink you could ever consume. The leucine in the BCAAs act as a permissive signal that tells your metabolism that amino acids are available so protein synthesis increases.

I am determined to protect my eyesight. Macular degeneration is the leading cause of blindness among the aged. The doses of leutin and zexanthin in Guardian are higher than the amounts shown to be effective in delaying or preventing macular degeneration in the famous ALRED trials. You will also be getting a bit more than 2 grams of Vitamin C a day if you take two packets as I do, another important protector of eye health (the eye has the highest concentration of Vitamin C of any tissue in the body for good reason since the eye is exposed to intense light and oxidation).

A few points on the value of BCAAs.

BCAAs appear to have unique obesity-related effects. BCAAs, and in particular leucine, increase fat leptin secretion, decrease food intake and body weight via mTOR signaling, and improve muscle glucose uptake and whole body glucose metabolism.

A promising area of preclinical research is regarding the effects of BCAAs on skeletal muscle atrophy. BCAA intake preserves muscle fiber size and improved physical endurance and motor coordination in middle-aged mice. Accordingly, an amino acid mixture with BCAA composition has been found to improve sarcopenia, i.e., the aging-associated loss of muscle mass, an effect possibly due to the recovery of the altered Akt/mTOR signaling in muscles of aged rats. BCAA supplementation increased the average lifespan of male mice.

A variety of amino acid mixtures have been used to restore the protein content of defective tissues, especially of skeletal muscles, in aged subjects. Dillon et al. reported that 3-month supplementation with essential amino acids increases IGF-1 muscle levels and lean body mass in aged women, without affecting kidney function. The acute anabolic response to this supplementation (increased muscle protein fractional synthesis rate) was maintained over time, suggesting the possibility to improve skeletal muscle trophism in long-term treatment.

Various BCAA dietary supplements have been reported to reduce sarcopenia in elderly subjects. In a randomized trial involving 41 subjects with sarcopenia aged 66 to 84 years, intake of the BCAA formula increased muscle mass, reduced tumor necrosis factor-α, and improved insulin sensitivity.

Most importantly, leucine-enriched balanced amino acid supplements are now considered as part of the nutritional recommendations for the management of sarcopenia.

References and further reading

Lash, L. H. L. (2005). Role of glutathione transport processes in kidney function. Toxicology and Applied Pharmacology, 204(3), 14–14. doi:10.1016/j.taap.2004.10.004

Lash, L. H. (2006). Mitochondrial glutathione transport: Physiological, pathological and toxicological implications. Chemico-biological interactions, 163(1-2), 14–14. doi:10.1016/j.cbi.2006.03.001

Lash, L. H., & Jones, D. P. (1984). Renal glutathione transport. Characteristics of the sodium-dependent system in the basal-lateral membrane. Journal of Biological Chemistry, 259(23), 14508–14514.

D'Antona, G., Ragni, M., Cardile, A., Tedesco, L., Dossena, M., Bruttini, F., et al. (2010). Branched-chain amino acid supplementation promotes survival and supports cardiac and skeletal muscle mitochondrial biogenesis in middle-aged mice. Cell Metabolism, 12(4), 362–372. doi:10.1016/j.cmet.2010.08.016.
This study finds that BCAA supplementation increased the average life-span of mice.

Valerio, A., D'Antona, G., & Nisoli, E. (2011). Branched-chain amino acids, mitochondrial biogenesis, and healthspan: an evolutionary perspective. Aging …, 3(5), 464–478.

Shimomura, Y., Murakami, T., Nakai, N., Nagasaki, M., & Harris, R. A. (2004). Exercise Promotes BCAA Catabolism: Effects of BCAA Supplementation on Skeletal Muscle during Exercise. The Journal of Nutrition, 134(6), 1583–1587.

Shimomura, Y., Yamamoto, Y., Bajotto, G., Sato, J., Murakami, T., Shimomura, N., et al. (2006). Nutraceutical Effects of Branched-Chain Amino Acids on Skeletal Muscle. The Journal of Nutrition, 136(2), 529–532.

Wu, G., Fang, Y.-Z., Yang, S., Lupton, J. R., & Turner, N. D. (2004). Glutathione Metabolism and Its Implications for Health. The Journal of Nutrition.

I have put up some of my many interviews over at the Media link on the header.

Glutamate is known as glutamic acid. This substance appears in most modern, manufactured foods. It appears as “flavor enhancer” in many manufactured foods, the acid is added to soft drinks to give them “zing”, and is the toxic component of MSG, the favored flavor enhancer of many Asian foods. Soy and grains have a large dose of glutamate. Cheese and other dairy foods are also a source.

Foods that are high in glutamate or glutamic acid include nearly everything served in fast food restaurants --- sauces, chips and dips, soups, cold cuts, low and non-fat milk, nutrasweet, aspartame, diet drinks, artificially sweetened desserts. Many seasonings consist of protein hydrolysates that contain free glutamic acid. They act like MSG, but are given a clean label by the FDA. Most french fries contain glutamic acid or these hydrolyzed proteins as “flavoring”. Even WW’s favorite cheese, parmesan, is high in MSG naturally. Very ripe tomatoes are high in glutamate. Body builder protein drinks are high in free glutamate. Casein is 20% glutamic acid. Whey is extremely high in glutamic acid. Sea salt is loaded with glutamate.

While fast food has been demonized for its fat content, it may be that the glutamic acid is more damaging.
 
Next to lectins, glutamate may be one of the most troubling proteins in the deadly grains. 35% of the protein in wheat is glutamate. Gluten grains, corn, soy and dairy are to be avoided for many reasons, but one of the most important is that they are high in glutamate.

Meat is relatively high in glutamate, but it is bound with other amino acids and is not set free as free glutamate unless the meat is cooked slowly. Slow cooking hyrolyzes the proteins and releases free glutamate. So, cook meat on the BBQ and sautee’ seafoods. If you eat meat or seafood without all the other sources of glutamate, such as the NED, you rid yourself of the potential for glutamate toxicity.

Now, what about the science of glutamate toxicity? In “Oxidative glutamate toxicity involves mitochondrial dysfunction and perturbation of intracellular Ca2 + homeostasis” published in Neuroscience Research 37 (2000) 227–236 we find that mitochondrial stress is induced by glutamate above physiological levels.

Their conclusion is “In conclusion, our data indicate that glutamate, at concentrations which block cystine uptake in PC12 cells leading to GSH depletion and inducing oxidative stress, increases ROS accumulation and decreases cell survival by a mechanism involving mitochondrial dysfunction and impairment of Ca2+ homeostasis.”

To expand on that a bit, the authors introduce their article thusly: “Oxidative stress is thought to be related to various neurodegenerative conditions and disorders including ischemia-reperfusion, traumatic injury, Parkinson’s disease (PD) and Alzheimer’s disease (AD) (Kehrer, 1993; Jenner, 1994; Bolan et al., 1997). The amino acid glutamate may induce oxidative stress in neurons and has been implicated in various neurodegenerative diseases (Coyle and Puttfarcken, 1993; Lees, 1993; Blandini et al., 1996; Obrenovitch and Urenjak, 1997).”

More from the authors, “The competition by glutamate for the cystine/glutamate antiporter induces an imbalance in the homeostasis of cystine, the precursor of glutathione (GSH). Therefore, the inhibition of cystine uptake by the constant and high exposure to glutamate is supposed to give rise to an inability to maintain intracellular GSH levels, leading to a reduced ability to protect against oxidative injury of the cell and, ultimately, cell death. The accumulation of an excess of free radicals seems to be responsible for the toxicity, because this second pathway can be blocked by antioxidants (Miyamoto et al., 1989; Davis and Maher, 1994).”

The bottom line is that glutamate causes a depletion of the essential GSH antioxidant and promotes the entry of calcium into the cell which turns on the cell death program. To quote the authors in conclusion: “It is clearly demonstrated that high glutamate concentrations induce cell death through a mechanism involving an increase in the levels of reactive oxygen species (ROS) as a consequence of intracellular GSH depletion, which leads, through mitochondrial dysfunction and perturbation of intracellular Ca2+ homeostasis, to cell death.”

How much do I worry about all this? Not much, because of my high intake of the Ultrathione GSH in Guardian and virtually zero intake of processed foods or body builder supplements. My diet elimates the other sources, such as soy, milk, cheese, and grains, beans, peanuts. I eat only moderate amounts of nuts. Never seeds. One of the little-known elements of eating Paleo is that you avoid nearly all of these sources of free glutamate or glutamic acid. Just don't stew your meat or eat meat loaf.

The prevailing view is that the limiting factor in prolonged exercise is the amount of glycogen stored in the working muscles. But, the research continues to challenge this established position and the simple theory offered to support it. The theory is that the more glycogen you have stored in muscle, the longer you can run or cycle or do useful work. The simple theory is wrong because it does not incorporate the feed back loops and adaptations that occur in energy use and muscle enzymes when you change to a low carb diet. Second order effects are often ignored in theories of physical performance and this is just another instance of that.

The experiments described in the article by Miller and Bryce. “Adaptations to a high-fat diet that increase exercise endurance in male rats.” Journal of Applied Physiology (1984) vol. 56 (1) pp. 78-83 refute the simple theory. So compelling are these results that lard manufacturers may start advertising their products as performance fuels. The rats fed lard in this experiment far out performed the rats fed a high carbohydrate diet.

From Miller and Bruce, “First, we wanted to know the effects of a LCD on liver glycogen content in rats, because this aspect had not been investigated previously. Also, if a LCD could sustain endurance exercise, we wanted to know what physiological or biochemical adaptations might explain this phenomenon.”

The authors created two groups of rats---one on a diet of 11% fat, 20% protein, and 69% carbohydrate. The low carbohydrate diet (LCD) fed to the other group contained 78% fat, 21% protein, and 1% carbohydrate. Both diets contained equal energy and both were supplemented with vitamins and minerals.

In their discussion, the authors note the following:

• Rats on a LCD for as little as 1 wk or as long as 5 wk can run significantly longer than those on a ND, despite reduced glycogen storage. This is contrary to the prevailing theory in the literature.
• A short-term LCD (3-7 days) reduces endurance time to exhaustion and decreases exercise performance, but a long-term LCD has the opposite effect. So, a lot of the concern for glycogen “replacement” is based on defective research that did not allow sufficient time for adaptation to the LCD.
• The LCD rats had far lower muscle and liver stores of glycogen but ran significantly longer, showing glycogen stores are not essential to endurance.
• The rats on the LCD had lower lactate and ketone levels, showing they were operating on these alternative fuels.
• They also had lower blood glucose and I would assume they had lower insulin too. Their muscle enzymes adjusted to utilize fat and conserve glycogen as a fuel.
• The muscle tissues adapt to the LCD to improve oxidative capacity when little carbohydrate is available.
• After the first week, the LCD rats ran 8% longer and after 5 weeks they ran 33% longer.
• The LCD contained the same energy content as the ND, but the rats were bigger at the end of 5 weeks on the LCD, which means that their adaptation was even greater since they carried more mass as they ran.

As for me, there is no lard in my performance diet and I think that over a longer time period the LCD diet might induce some unfavorable adaptations not investigated in this study. Note that these rats were not able to eat more calories on either diet, but over a longer time course and more abundant food, the caloric content of the diets would diverge and the LCD diet might induce weight gain relative to the ND. Or the other way around. I don't think we know.

The anti-aging effects of caloric restriction (CR) are still being investigated. The effects of CR are not well understood even though it is known to extend life in some species and improve markers of health. In EF (Evolutionary Fitness), we do not do chronic CR. Instead we do intermittent fasting (IF) and we restrict glucose. We strive for low insulin, which glucose and simple starch restriction partly achieve. In addition, we undergo acute energy restriction through high intensity exercise. Exercise of this form does not promote ROS formation in the mitochondria, at least not at the same rate that aerobic exercise is known to do. I think we understand that glucose was the signal during evolutionary times of energy abundance and that insulin, along with IGF-1, is the metabolic pathway of signals that promoted growth and reproduction over maintenance. That means that glucose restriction may be as effective as CR in promoting longevity.

This argument is not easily settled: is it CR or glucose restriction that enhances longevity? One of the ways to resolve this is to look at the effect of insulin on the production of ROS (reactive oxygen species) in the mitochondria. It turns out that insulin reverses the beneficial effects of CR on mitochondrial production of ROS. So, CR may not reduce ROS formation in the mitochondria if glucose and simple starches are part of the diet. This means, I think, that the restriction of glucose and the reduction of stored glucose in the muscle (as glycogen), both key components of EF, is a clear winner over CR in promoting longevity. We don’t have to experience the misery of chronic CR, with its hunger and mood-altering effects, to enjoy a longer life. We just cut the glucose and keep our insulin low.

Here is an abstract that describes the effect of insulin in CR on the production of ROS by mitochondria.

Lambert et al. Exogenous insulin can reverse the effects of caloric restriction on mitochondria. Biochemical and biophysical research … (2004)

It has been proposed that part of the anti-aging mechanism of caloric restriction (CR) involves a reduction in both the generation rate of reactive oxygen species (ROS) by mitochondria, and a reduction in peroxidizability of mitochondrial membranes. It was hypothesized that these effects may be due to upstream changes in hormonal status, since certain hormones (such as insulin) are stimulatory for ROS production, effect fatty acid composition, and are lowered by CR. To investigate this hypothesis, young male Brown–Norway rats on 55% CR (4 months duration) were subjected to insulin replacement by use of mini-osmotic pumps. ROS and free radical-induced malondialdehdye production were significantly lower in mitochondria from CR animals compared to those from fully fed, and these effects were reversed by insulin. It is concluded that the beneficial changes induced by CR, as seen at the mitochondrion, may in part be downstream effects of alterations in hormonal signalling.

From Isganaitis and Lustig. Fast food, central nervous system insulin resistance, and obesity. Arteriosclerosis (2005) is this important finding.

In rats, hyperinsulinemia increases expression of a glucose transporter (GLUT4) in adipose tissue while decreasing expression of this same transporter in muscle, demonstrating that excess insulin can simultaneously foster insulin sensitivity in fat while triggering resistance in other tissues.

Recall one of the points I made in my conclusion to the series The Fundamental Dynamic of Life where I stated:

• Insulin receptor activity in muscle is stronger than in fat tissue when receptors are under low oxidative stress. That means that when you are inflamed or have low oxidative defenses, the energy you consume becomes more available to your fat cells than to your muscle cells. This goes back to the “competition within” that I spend a chapter in my book on. Tipping into the oxidative stress state alters the competition between fat cells and muscle cells for energy in favor of fat.

So, a lesson is that hyperinsulinemia, which fosters oxidative stress, can increase sensitivity in fat while causing insulin resistance in muscle. It is what your metabolism does with what you eat that matters. Lose your resistance to oxidative stress, eat meals that make you hyperinsulemic, and watch your fat capture more of what you eat than your muscle.

It is well-known that fat people do not fidget as much a lean people do. I had a funny illustration of that point today as I sat on my patio reading Kahneman's Thinking, Fast and Slow. There was a golf tournament going on and a foursome played through two holes as I watched.

Three were neither fat nor lean, but one was quite fat. His belly protruded over his belt dramatically. As the foursome stood on the green to putt, three of them walked around studying lines and whatever they study. The fat guy just stood there.

They got in their carts and drove to the next hole. Three guys got out and fidgeted with their clubs, balls and tees and practiced swings as the foursome ahead putted out. The fat guy sat in his cart and waited until it was his turn to get out and swing. The same scene unfolded on the next green.

The fat guy never fidgeted the way everyone else did. He did not "waste" energy the way the others did, even though he had no need to conserve energy since he carried at least twice as much energy as the others. So, is he fat because he does not fidget and use energy the way the others do? Or, does he not fidget because he is fat? I don't think the first explanation works because it fails to explain the lack of fidgeting and subscribes to some version of the energy balance model. I happen to think that he does not fidget because he is fat.

I know it seems paradoxical, but I think the explanation may be that the fat guy's brain is under far more energy stress than the others' brains are because there is less competition for energy from a large mass of fat tissue that the fat guy carries. His fat is stealing energy from his brain and his brain senses that and curtails fidgeting and minimizes movement.

I have been asked about what I look like from the front. This is not a recent picture, but it is all I have. It is about 4 years old, so am about 72 in this picture. My hair is longer now and I have fewer wrinkles than I had when this was taken. Today, I weighed 204.8 pounds at 8% body fat. It is time to end this as I do not want it to be anything more than simple reporting. The large scar on my left shoulder is from a crash in a cross-country motorcycle race deep in the woods and mud of Texas back when I was a professor there.