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.

 


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