That's the Issue...G-Flux: E ≠ MC2

As any gurrlll will tell ya -- certain times of the month (e.g. when we're bleeding down our legs) no matter what we eat/don't-eat, girls gain %^&*$weight. Yet... at other times...we gals can eat E-V-E-R-Y-T-H-I-N-G in sight... and... drop pounds... have more energy... more shredding/shedding.

What's the issue...??

Human bodies do not obey the laws of matter and physics. Esp... girls... *wink* We break all the metabolism rules... and hormones fluctuate. Unlike physical matter, hormone-cascades rule energy flux, flow and balance.



Biological Energy Turnover

Often like life... the more you give, the exponentially more . . . you get.

Energy in alive, biological systems appears to follow the same rule, to me. With more propelling exercise and intense power demands, the human body is the greatest machine to turn over and kick out more outputs than inputs. Mitochondria, our tiny nuclear power-generating plants, double...or even...QUINTUPLE in quantity and quality for future expected thermodynamics. (Conversely, they are degraded with 'hibernation signals' -- insulin, low thyroid, movement-deficiency + subsequent T, hGH, adiponectin hormone declines, high carbs, high F**C-tose, x-s omega-6 veggie oils, diminished daylight/Vitamin D deficiency, EPA+DHA insufficiency, micronutrient/co-factor deficiencies, etc.)




Frank Starling's Rule...of Heart/Muscles Biophysics:

Max Cardiac Output = Max Heart Rate X Max Stroke Volume

For us Paleo people, during functional, natural exercise, how does the heart provide so much ATP, energy packets, with constant and high outputs? At high intensity efforts...like Tabata squats? 100 burpee-pullups? interval 400m sprints? Oly-weight-lifting like dead-lifts and power cleans 8 x3...?? Which then translate effortlessly (without practicing) to faster running, flying across hills, and jumping to never imagined heights...!? I n d e e d y . . . Olympic-lifting explodes vertical-leaping and bounding better than... Superman himself. Another one of our important muscles, the heart, works the same way. It is a muscular biological pump. How strong the heart can pump blood-volume and how efficiently oxygen is supplied are the factors that determine the max work and max volume delivered with every heartbeat. See above Frank Starling formula. With the proper training, the heart muscle cells in fact grow BIGGER (yea)... THICKER (yea-aaahh) with mitochondria, the ATP-power-generators... MORE EQUIPPED with enzymes and co-factors to transfer energy -- fatty acids, lactate, glycogen/glucose -- and to increase 'end-products' neutralizers (Coenzyme Q10).

Our heart cells (cardiomyocytes) are one of nature's best examples of bio-engineering for structure, composition and mechanical genius. They beat for you every second...of your life ~100,000 times per day.

Unless you are . . . Lance . . . only ~46,000 times per day at rest. Uuummm...I'd like to see...umm I mean... study... his... drool-inducing PPARs... *wink* I hear he's finally picking up kettle balls...
What maintains energy supply at peak aerobic exercise in trained and untrained older men? Amir R et al. Gerontology. 2007;53(6):357-61.


In an untrained heart, the volume of mitochondria take up ~5% of the cell. However, in hearts of athletes, mitochondria reside in as much as 20-25% of the heart cell. That is five-times more massive...! Harness the power of your mitochondria... by optimizing your G-flux (see below about energy flow).

Maximal cardiac output increases in response to exercise training. Intensity determines how fast this happens.

In fact excessive endurance exercise (see below 24-h trained endurance results) worsen oxygen efficiency in mitochondria. Short intense, resistance, interval exercise on the hand produce quick generation of mitochondria in a few days, improved glucose utilization, insulin reduction, and activates PPAR-Delta, the switch for anti-inflammatory and pro-immunomodulatory actions in the body.
Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise. Sahlin K et al. J Appl Physiol. 2007 May;102(5):1844-9.
Regulation by exercise of skeletal muscle content of mitochondria and GLUT4.Holloszy JO. J Physiol Pharmacol. 2008 Dec;59 Suppl 7:5-18.
Exercise interval training: an improved stimulus for improving the physiology of pre-diabetes. Earnest CP. Med Hypotheses. 2008 Nov;71(5):752-61.
Regulation of muscle fiber type and running endurance by PPARdelta. Evans RM et al. PLoS Biol. 2004 Oct;2(10):e294.
Genetic variations in PPARD and PPARGC1A determine mitochondrial function and change in aerobic physical fitness and insulin sensitivity during lifestyle intervention. Häring HU et al. J Clin Endocrinol Metab. 2007 May;92(5):1827-33.
Mitochondrial myopathies: diagnosis, exercise intolerance, and treatment options. Tarnopolsky MA, Raha S. Med Sci Sports Exerc. 2005 Dec;37(12):2086-93. Review.
Resistance training, sarcopenia, and the mitochondrial theory of aging. Johnston AP, De Lisio M, Parise G. Appl Physiol Nutr Metab. 2008 Feb;33(1):191-9. Review.
Circuit resistance training in chronic heart failure improves skeletal muscle mitochondrial ATP production rate--a randomized controlled trial. Hare DL et al. J Card Fail. 2007 Mar;13(2):79-85.
Antioxidant enzyme activity is up-regulated after unilateral resistance exercise training in older adults. Parise G, Phillips SM, Kaczor JJ, Tarnopolsky MA. Free Radic Biol Med. 2005 Jul 15;39(2):289-95.
Muscle fat oxidative capacity is not impaired by age but by physical inactivity: association with insulin sensitivity. Morio B et al. FASEB J. 2004 Apr;18(6):737-9.
Strength and aerobic training attenuate muscle wasting and improve resistance to the development of disability with aging. Booth FW et al. J Gerontol A Biol Sci Med Sci. 1995 Nov;50 Spec No:113-9. Review.




What is the preferred energy source of heart and skeletal muscle cells?

Well...it certainly aint Gu or sports drinks or energy bars or carb-loading. As we exercise and become more trained, the preferred source for mitochondria is fatty acids...both our temporarily stored fats in skeletal muscle and the band of saturated fat across the heart...

"Proper heart function relies on high efficiency of energy conversion. Mitochondrial oxygen-dependent processes transfer most of the chemical energy from metabolic substrates into ATP. Healthy myocardium uses mainly fatty acids as its major energy source, with little contribution of glucose."
Metabolic and genetic regulation of cardiac energy substrate preference. de Jong JW et al. Comp Biochem Physiol A Mol Integr Physiol. 2007 Jan;146(1):26-39. Epub 2006 Oct 3. Review.


"Mitochondria in skeletal muscle tissue can undergo rapid and characteristic changes as a consequence of manipulations of muscle use (e.g. MOVEMENT...use it or lose it) and environmental conditions . . . Additionally, a shift of substrate metabolism toward a higher reliance on lipids is observed, structurally reflected as a doubling of the intramyocellular lipid content . . . Transcription factors AP-1 and PPARalpha/gamma and the protein kinase AMPK are signaling molecules that transduce the metabolic and mechanical factors sensed during endurance training into the complex transcriptional adaptations of mitochondrial proteins."
Plasticity of skeletal muscle mitochondria: structure and function. Hoppeler H, Fluck M. Med Sci Sports Exerc. 2003 Jan;35(1):95-104.




G-Flux: Building the Ultimate Body (excerpt)
by Dr John M Berardi (T-Nation.com)

What's G-Flux?

"Well, G-Flux, otherwise known as energy flux (or energy turnover) is the relationship between energy intake and expenditure. It's the balance between the two. Put another way, it's the amount of calories you "turn over". ...Having a high G-Flux is 100%, without a doubt, absolutely critical to building your ultimate body – which I'm assuming includes strong, functional, well-adapted muscle, low body fat, and great health."

Energy In ≠ Energy Out

That's the thermodynamic i-s-s-u-e . . .



G-Radio: 'That's the issue...SoulJaBoytellem...'
*air-kiss-u* ...hormones... philematology...another place ancestral hormonal pathways rule

Vitamin D: Nature's Antibiotic 20-50k IU daily x 3 days

FIG. 5. Antiinflammatory effects of vitamin D in the critically ill. Plasma concentrations of CRP and IL-6 serum concentrations over time in ICU are depicted for the two study groups. Open bars represent the low-dose 200 IU/d vitamin D group (n 10), and hatched bars represent the high-dose 500 IU/d group (n 12). Data are means SEM. Elevated CRP and IL-6 levels, observed on ICU admission, decreased significantly with time in ICU in both study groups. The fall in CRP was significantly more pronounced in the high-dose vitamin D group, compared with the low-dose group between d 3 and d 7; likewise in the high-dose group, IL-6 levels decreased from admission to d 4, whereas they remained unaltered in the low-dose group.
(*, P less than 0.05.)


I love vitamin D3 5000 IU from NOW brand in olive oil (iherb.com $8.80 per bottle of #120 capsules... at 12 bottles per case)...for optimal health and longevity *smile* and optimal flu/immunological protection)

ONE A DAY KEEPS THE PULMONOLOGIST AWAY...


And when I'm coming down with a cold . . . T-E-N (10) A DAY KEEPS THE FLU AWAY :)


In fact I've been using vitamin D as an antibiotic as well for the last 18 mos and have had very few colds. Prior to supplementation, I suffered from frequent URIs, coughing spells and bronchitis that would last 8wks or longer with little benefit from albuterol and steroid inhalers. (Lack of natural estrogen, suppressed by synthetic progestin, was the cause it turns out -- and yes the drug companies know this -- yes -- read the package insert of your contraceptive).

How do you know if you are vitamin D deficient? Frequent colds? Asthma? Hayfever/Allergies? Feel crappy, achy, sad sometimes? You probably have significant vitamin D deficiency. Most lab standard ranges post 'normal' vitamin D 25(OH)D as 30 to 100 ng/ml and this is clearly out dated and 'off.' Normal for outdoor living, non-makeup, non-sunscreen-wearing individuals is ~60-80 ng/ml, and this is what should be achieved via supplementation, sun and food (food is the poorest source unless you are Inuit on a high-fat-seal/seafood-diet). And...Forget about sunlight/UVB if you live away from the equator . . . y e s . . . that includes San Francisco and anything NORTH for about ~4-6 months per year.


Antibiotic dose ('Stoss' protocol): ~25,000 to 50,000 IU daily in the AM (or split) for 3 days

(Precise dose: 1000-2000 IU per kg (or 500 IU per ~pound))

Side Effects: wake up without sniffles, scratchy throat, green phlegm, chest tightness or asthma


The above study (graph) was a short one in a small number of critically ill patients. A 'high' dose vitamin D (only 500 IU/day) was more effective at lowering CRP, marker for inflammation, and IL-6, immune marker for infected-tissue destruction, compared with 'low' dose vitamin D (200 IU/day). What does this show? Not much except . . . (1) when one is critically ill the blood vitamin D concentration hit ROCK BOTTOM (why? it's nature's antiobiotic and restorative hormone) . . . and (2) even licking a vitamin D capsule will provide IMMENSE immunological benefit and may perhaps even save your life if you are ever critically ill.

As a kid one summer, I became almost critically ill after a mild-sized 3rd degree burn on my L-thigh (which I joking refer to as my 'shark bite' if people happen to ask). As a child, the area was a significant portion of body surface area and I was near comatose for a little while (my father doesn't even remember how long). Spending 24/7 outdoors in the hot humid Pennsylvania sun that summer prior to the accident probably provided some degree of vitamin D, I believe, to have afforded some protection, healing, and surviving (in addition to the antibiotics/steroids).
Bone turnover in prolonged critical illness: effect of vitamin D. PDF here. Van den Berghe G, Van Roosbroeck D, Vanhove P, Wouters PJ, De Pourcq L, Bouillon R. J Clin Endocrinol Metab. 2003 Oct;88(10):4623-32.



Below is info from Dr. Cannell and his non-profit Vitamin D Council on the curious antimicrobial protective effects and benefits of vitamin D.

May you and your family allude the flu this season!



http://www.vitamindcouncil.org/newsletter/2006-june-july.shtml

Is Vitamin D An Antibiotic?

Antimicrobial Peptides

"Dr. Liu and colleagues at UCLA, publishing in this March's edition of the prestigious journal Science, showed that vitamin D might be, in effect, a potent antibiotic. Vitamin D increases the body's production of naturally occurring antibiotics: antimicrobial peptides. Antimicrobial peptides are produced in numerous cells in the human body where they directly and rapidly destroy the cell walls of viruses and bacteria, including tuberculosis. Furthermore, Liu showed that adding vitamin D to African American serum (African Americans have higher rates of TB) dramatically increased production of these naturally occurring antibiotics.

Liu PT, Stenger S, Li H, Wenzel L, Tan BH, Krutzik SR, Ochoa MT, Schauber J, Wu K, Meinken C, Kamen DL, Wagner M, Bals R, Steinmeyer A, Zugel U, Gallo RL, Eisenberg D, Hewison M, Hollis BW, Adams JS, Bloom BR, Modlin RLToll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006 Mar
24;311(5768):1770–3.


Plenty of you have e-mailed me that pharmacological doses (high doses) of vitamin D (1,000–2,000 units/kg per day for three days), taken at the first sign of influenza, effectively reduces the severity of symptoms. However, has anyone ever studied giving 100,000, 200,000, or 300,000 units a day for several days to see if vitamin D induces antimicrobial peptides to help fight other life-threatening infections? (By the way, doses up to 600,000 units as a single dose are routinely used in Europe as "Stoss" therapy to prevent vitamin D deficiency and have repeatedly been shown to be safe for short-term administration.) No, you say, studies of "Stoss" therapy in serious infections have never been studied or reported in reputable journals. Well, maybe such treatment has been studied—and reported in the best journals—by way of the weirdest medical invention ever patented in the USA."

Dr.Mao, Brain Foods, Autism, And Alzheimer's Prevention

I like Dr. Mao for his quickie Yahoo tidbits... His advice is great! And very aligned to TrackYourPlaque and longevity as well. Sometimes I wonder what's more important...our brain or our heart? Or the vasculature which is what we 'track' at TYP...? I'm grateful actually that ALL in fact improve exponentially with the same program.

How w o n d e r f u l can life be?!?

G-radio:Mraz 'Wonderful Life' *wink*

All the foods and nutrients listed below are inherent ingredients to our TYP heart reversal stories, "essential amino acids, omega oils, minerals and vitamins":
--Taurine from wild seafood and grassfed meat (not found in veggies)
--Arginine
--Other proteins: Leucine, BCAA, L-Carnitine, etc
--Omega-3 fatty acids: EPA DHA (grassfed meat, seafood); ALA (almonds, flax)
--Omega-6 fatty acids: GLA (sesame oil, borage, primrose, hemp)
--Minerals: Magnesium, Iodine, Selenium, Zinc, Boron, Sulfur, etc
--Vitamins: Vitamin D (calcidiol), Vitamin A, Vitamin E (tocotrienols), Vitamin K1 K2 (esp MK7), methylated folic acid, B-vitamins, Niacin (B3), B6/B12/folate/TMG (homocysteine control), acetylated a-Lipoic Acid, etc
--Antioxidant Flavanoids: blueberries, green tea, pycnogenol, red wine, bilberry, et cetera


8 Foods to Keep Your Brain Young and Healthy

By Dr. Maoshing Ni - Posted on Mon, Aug 11, 2008, 1:42 pm PDT

Senility, Alzheimer's, and age-related memory loss: these conditions of mental decline that come with aging can be delayed or even prevented. Besides engaging in daily activities that work out your brain, a regular and balanced diet rich with essential amino acids, omega oils, minerals and vitamins will ensure a vibrant and sharp memory. Eat these foods to give your brain the nutrition it needs.

1. Fish
Protein, an important component in the making of neurotransmitters, is essential to improve mental performance. Aside from being an excellent source of high quality protein, fish are packed with essential oils, such as Omega-3, which protect the brain and supports its development and functioning. Deep sea fish have the highest amounts of fatty acids, and they include salmon, sea bass, halibut, mackerel, and sardines.

2. Blueberries
These delicious berries are full of powerful antioxidants, which eliminate free-radical damage that causes aging, and they also possess neuroprotective properties that can delay the onset of age-related memory loss by guarding brain cells from damage caused by chemicals, plaque, or trauma. And they combat inflammation, the other factor in aging. 3. Nuts and SeedsNuts and seeds are wonder foods for your brain. Packed with protein and essential fatty acids, nuts and seeds are also chock full of the amino arginine, which stimulates the pituitary gland at the base of the brain to release growth hormone, a substance that declines quickly after age 35; this is a real anti-aging boon to your brain! Whip up a batch of my "Anti-aging brain mix" to bring with you anywhere and eat a small handful in between meals as a daily snack. It will nourish and support your brain. Pack in sealed container or zip-lock bag to preserve freshness.
1 cup walnut
1/2 cup pine nuts
1/4 cup sesame seeds
1/2 cup pumpkin seeds
1/3 cup of dried goji berries (also known as lycium berry, and easily found in health food stores)
1/2 cup dried apricots

4. Cruciferous Vegetables
Broccoli, cauliflower, and Brussels sprouts are all rich in choline, an essential nutrient for memory and brain health. Choline is a precursor to the neurotransmitter acetylcholine, which contributes to healthy and efficient brain processes. As we age, our body's natural choline output declines, and its neurochemical action weakens. You can eat choline-rich foods to increase your production of acetylcholine, which will improve your brain power. Other sources of choline include: eggs, soybeans, peanuts, cabbage, black beans, and kidney beans.

5. Oil: Monounsaturated Fats
Monounsaturated fats contain essential fatty acids and gamma-linolenic acid (GLA), which are crucial for brain development and function, among many other excellent benefits for your health. Olive oil, sesame oil, canola oil, almond oil, flaxseed oil, and fish oil are rich in monounsaturated fats and are good choices for brain health. Population studies show that people with a diet that is high in unsaturated, unhydrogenated fats may have a reduced risk of Alzheimer's disease, whereas those with a diet that is higher in saturated fats and trans fats have an increased risk.

6. L-carnitine Foods
Age-related memory problems are many times caused by plaque buildup and diminished blood supply to the brain, compromising the delivery of nutrients and oxygen. L-carnitine, an amino acid manufactured in your liver, increases circulation in the brain — among a myriad of powerful benefits for your health. Also, because it prevents fat oxidation in the brain, L-carnitine shows some promise in preventing Alzheimer's disease. Good sources of L-carnitine include: meats, fish, poultry, wheat, avocado, milk, and fermented soybeans.

7. Microalgae
Microalgaes from the ocean and uncontaminated lakes, including blue-green algae, spirulina, chlorella, seaweed, and kelp are easy-to-digest, high protein and high-energy supplements-and contain over a hundred trace minerals! Available in your health food store, microalgae are simple to incorporate into your diet to ensure a good, strong brain function. Look for powders you dissolve in juice or flakes you can sprinkle on your food.

8. Green Tea
Green tea prevents an enzyme found in Alzheimer's disease and is also rich in polyphenols, antioxidants that help prevent premature brain aging. Drink two cups a day to get the brain benefits. To decaf tea, steep for 45 seconds and pour out the water, add fresh hot water to the leaves or tea bag — 95% of caffeine will be eliminated.

Ketogenic Diet for Alzheimer's and other Neuro-degenerative/Vascular Diseases

Why is a ketogenic diet effective for neurodegenerative and vascular diseases (like CAD)? I've wondered this since Atkin's became so popular. I've also wondered why such extreme improvements are noticed short- and long-term with Niacin (Vitamin B3; we use either Slo-Niacin or Niaspan at TYP). This one incredible addition to any heart program evolves dramatic plaque remodelling, heart disease reversal, lipoprotein turn-arounds and large ranges of CAC score regressions. In the HATS trial in post-MI patients, Niacin + simvastatin 40mg/d brought about a 90% reduction in mortality and CAD events in ~3yrs compared with placebo. That is quite dramatic. The results are unheard of for conventional, pharmaceutical-derived therapies. Statin-monotherapy brings about only 20-30% depending on the study...which again as the latest WSJ article summarized...so what? These days when individuals carry belly fat and have elevated insulin, heart attacks and coronary surgical interventions are more de rigueur than NAUGHT... despite statins being placed in the water by health care insurances and people's demands.

What is niacin? Niacin mimics 2 things: starvation (living off your body fat/rearend) and ketosis. Niacin binds the ketone body receptor known as PUMA-G. Ketones are generated under many circumstances for instance:
--first 2 weeks of an infant's life -- baby is living on 60-80% brown fat because momma has not produced enough milk yet (as time is required for those lactative n*pples to so-called 'callous up' -- yeah, men out there that is JUST LIKE running a marathon without bandaids on your b**bies *haaa ah* seriously... bloody...d*mn...fun...)
--starvation (think, Survivorman or Bear)
--intermittent fasting (2-4x/wk 18 to 36 hour fasts)
--12-hour fasts (like for the doctor-ordered cholesterol lab testing)
--physical training beyond 40-60min (eg, sex typically does not count)
--low carb diet
--no carb diet
--moderate to high fat (low carb) diet
--moderate to high protein (low carb) diet
--Paleo + IF (intermittent fasting) + exercise


Don't confuse ketosis with Type 1 diabetes DKA (diabetic ketoacidosis) which is highly fatal. Many doctors and other healthcare professionals do this. It is like comparing normal wear-tear like a shopping cart scratching your car versus a 20-car wreck involving multiple fatalities. Ketosis is in fact normal and part of evolution. Humans and other predators up on the food pyramid of life do it all the time. Ketosis is necessary for survival.

The situation known as DKA occurs because the individual has ZERO insulin. Don't worry -- unless Type 1 or 1.5 (LADA) Diabetes is present, we all make plenty of insulin to 100% prevent this. In fact most people produce far too much insulin which raises blood pressure, causes body fat weight gain, TGs, small dense LDL and other inflammatory markers. Too much insulin also hinders proper muscle development (hard-gainers) with resistance and weight training. (DKA may occur but is VERY very rare in Type 2 diabetes -- unless the person has an infection or sepsis.)




Ketones Fix Our Brain

Altered lipid metabolism in brain injury and disorders.
Adibhatla RM, Hatcher JF.
Subcell Biochem. 2008;49:241-68. Review.

Department of Neurological Surgery, Cardiovascular Research Center, Neuroscience Training Program, University of Wisconsin School of Medicine and Public Health, Madison, WI., William S. Middleton Veterans Affairs Hospital, Madison, WI 53792, USA.

Deregulated lipid metabolism may be of particular importance for CNS injuries and disorders, as this organ has the highest lipid concentration next to adipose tissue. Atherosclerosis (a risk factor for ischemic stroke) results from accumulation of LDL-derived lipids in the arterial wall. Pro-inflammatory cytokines (TNF-alpha and IL-1), secretory phospholipase A2 IIA and lipoprotein-PLA2 are implicated in vascular inflammation. These inflammatory responses promote atherosclerotic plaques, formation and release of the blood clot that can induce ischemic stroke. TNF-alpha and IL-1 alter lipid metabolism and stimulate production of eicosanoids, ceramide, and reactive oxygen species that potentiate CNS injuries and certain neurological disorders. Cholesterol is an important regulator of lipid organization and the precursor for neurosteroid biosynthesis. Low levels of neurosteroids were related to poor outcome in many brain pathologies. Apolipoprotein E is the principal cholesterol carrier protein in the brain, and the gene encoding the variant Apolipoprotein E4 is a significant risk factor for Alzheimer's disease. Parkinson's disease is to some degree caused by lipid peroxidation due to phospholipases activation. Niemann-Pick diseases A and B are due to acidic sphingomyelinase deficiency, resulting in sphingomyelin accumulation, while Niemann-Pick disease C is due to mutations in either the NPC1 or NPC2 genes, resulting in defective cholesterol transport and cholesterol accumulation. Multiple sclerosis is an autoimmune inflammatory demyelinating condition of the CNS. Inhibiting phospholipase A2 attenuated the onset and progression of experimental autoimmune encephalomyelitis. The endocannabinoid system is hypoactive in Huntington's disease. Ethyl-eicosapetaenoate showed promise in clinical trials. Amyotrophic lateral sclerosis causes loss of motorneurons. Cyclooxygenase-2 inhibition reduced spinal neurodegeneration in amyotrophic lateral sclerosis transgenic mice. Eicosapentaenoic acid supplementation provided improvement in schizophrenia patients, while the combination of (eicosapentaenoic acid + docosahexaenoic acid) provided benefit in bipolar disorders. The ketogenic diet where >90% of calories are derived from fat is an effective treatment for epilepsy. Understanding cytokine-induced changes in lipid metabolism will promote novel concepts and steer towards bench-to-bedside transition for therapies.
PMID: 18751914

Ketogenic Diet Appears to be Neuroprotective For Alzheimer's

The below authors state that "the Ketogenic diet appears neuroprotective, promoting enhanced mitochondrial function and rescuing adenosine triphosphate production" and suggest the value for broad range applications including not just neurovascular conditions but also cancer. We worry about mitochondrial function at TrackYourPlaque (at least I do anyway :) but many others are getting keen to this disorder). Mitochondria are our little nuclear powerhouses that produce our energy currency, e.g. energy packets known as ATP. Mitochondrial dysfunction is what distinguishes many diseases including how gets mercury/aluminum-toxic/brain-damaged from vaccines in children. Read opinions by Seth Roberts PhD HERE (author of the Shangri-La diet, UCB Psychology professor emeritus). Dr.Roberts shares his insightful thoughts and n=1 experiments on brain function and many other topics, including the benefits of fermentation/probiotics. Many TYP members have tried the SLD (not... 'LSD') and lost significant weight with extra light virgin olive oil. It will be very fascinating to see what conclusions will result from examining probiotics. Short-chain saturated fatty acids (SCSFAs: butyrate, propionate, etc) are binders and activators of PPAR-delta, a potent inflammatory and immunomodulatory switch. SCSFAs are produced by anaerobic fermentation and perhaps may be the ingredients that exert the health and longevity benefits of cheese, natto, stinky tofu, yogurt, etc (Nilssen N dissertation). (interestingly...monounsaturated fatty acids in EVO in fact bind PPAR-delta and other PPAR receptors; ketones=beta-hydroxybutyrate indirectly also activates PPAR-delta).
The ketogenic diet: uses in epilepsy and other neurologic illnesses.
The neuropharmacology of the ketogenic diet.
The ketogenic diet and epilepsy. This therapy has been around 80++ yrs.
Progress in neuroprotective strategies for preventing epilepsy.
From clinical evidence to molecular mechanisms underlying neuroprotection afforded by estrogens.





Neuroprotective and disease-modifying effects of the ketogenic diet.
Hartman AL et al. Behav Pharmacol. 2006 Sep;17(5-6):431-9. Review. Free PDF
Below Excerpt

Alzheimer’s disease
Recent studies have raised the possibility that the ketogenic diet could provide symptomatic benefit and might even be disease modifying in Alzheimer’s disease. Thus, Reger et al. (2004) found that acute administration of medium-chain triglycerides improves memory performance in Alzheimer’s disease patients. Further, the degree of memory improvement was positively correlated with plasma levels of β-hydroxybutyrate produced by oxidation of the medium-chain triglycerides. If β-hydroxybutyrate is responsible for the memory improvement, then the ketogenic diet, which results in elevated β-hydroxybutyrate levels, would also be expected to improve memory function. When a patient is treated for epilepsy with the ketogenic diet, a high carbohydrate meal can rapidly reverse the antiseizure effect of the diet (Huttenlocher, 1976). It is therefore of interest that high carbohydrate intake worsens cognitive performance and behavior in patients with Alzheimer’s disease (Henderson, 2004; Young et al., 2005).

It is also possible that the ketogenic diet could ameliorate Alzheimer’s disease by providing greater amounts of essential fatty acids than normal or high carbohydrate diets (Cunnane et al., 2002; Henderson, 2004). This is because consumption of foods or artificial supplements rich in essential fatty acids may decrease the risk of developing Alzheimer’s disease (Ruitenberg et al., 2001; Barberger-Gateau et al., 2002; Morris et al., 2003a, b)...


Carbohydrate restriction as a protective mechanism

A key aspect of the ketogenic diet is carbohydrate restriction. The role of decreased carbohydrates in neuroprotection has been investigated through the use of 2-deoxy-d-glucose (2-DG), a glucose analog that is not metabolized by glycolysis. Lee et al. (1999) found that administration of 2-DG to adult rats at a nontoxic dose (200 mg/kg) for 7 consecutive days produced dramatic protection against hippocampal damage and functional neurological deficits induced by the seizure-inducing excitotoxin kainate. In addition, 2-DG was protective against glutamate-induced and oxidative stress-induced neuronal death in cell culture. The authors also found that reduced glucose availability induces stress proteins, including GRP78 and HSP70, which they proposed act to suppress ROS production, stabilize intracellular calcium, and maintain mitochondrial function..

Why this approach fixes and protects our brain...Cellular mechanisms underlying the neuroprotective activity of the ketogenic diet:
--Reverses damage on energy metabolism
--Reduced glutamate-mediated toxicity
--Normalization effects on γ-aminobutyric acid systems
--Enhances antioxidant mechanisms
--Protects against programmed cell death
--Carb restriction as a protective mechanism and less ROS






Mitochondrial Dysfunction, Heart Disease, and Autism

The Hannah Poling story is quite frankly riveting. This could have been our child. Or your child. After her 19-month vaccination series, Hannah started developing the signs and symptoms for autism, she stopped interacting with her world. Her father Dr. Jon Poling being an MD/PhD Neurologist is now trying to find solutions for not only his own daughter's recovery but also a whole legion of children of this Pharma vaccine-generation. Apparently Hannah exhibits a mitochondrial dysfunction which may be one of several factors (likely vitamin ADEK deficiency, wheat/gluten intoxication, omega-6 overdose and omega-3/saturated fatty acid insufficiency are all factors as well, imho, I'm not an autism expert yet).
Subpopulation of Mitochondrial Autism -- Autism Vox Blog
Jon S. Poling, MD, PhD (2006) -- Developmental Regression and Mitochondrial Dysfunction in a Child With Autism. Journal of Child Neurology, Vol. 21, No. 2, 170-172.


Interestingly, Heart Disease is implicated on the 'spectrum' of mitochondrial disorders. A statement from the United Mitochondrial Disease Foundation on the connection between mitochondrial disease and autism: “Recent published reports about the potential links between mitochondrial disorders and autism demonstrate the urgent need for more research into mitochondrial disease, a devastating and often fatal illness. Mitochondrial dysfunction has also been implicated in Alzheimer’s Dementia, Parkinson’s disease, Huntington’s disease, Heart Disease and Diabetes." It is not surprising to me. Individuals with heart disease often present themselves or their children with clinical autism or other conditions on the autistic spectrum: ADD, bipolar, major depression, schizophrenia. Perhaps mitochrondrial conditions are in fact woefully underdiagnosed. Aren't we all a little on the spectrum...?? I know I am not... the only one.



We Are Only As Strong as Our Weakest Mitochrondria

Mitochondria reside in all our alive cells (not hair or nails). They provide the energy needed for all energetic, metabolic and cellular processes. Honestly, if your car had no engine or an improperly functioning engine, how far do you think you will drive? Or at all?

Like our weakest link, sick mitochrondria bring us down.

How do we keep mitochrondria happy? Provide it the fuels it prefers. Give it the parts that need to be replaced upon damage/use. Don't throw cogs in its machinery.
--Fatty acids (mono-, saturated-, omega-3 long chained pufa, short-chained-saturated, medium- chained-saturated-, etc)
--Proteins
--Complex carbs (eg, vegetables)
--Coenzyme Q10 (involved in very last stop of ATP production)
--Alpha lipoic acid, Carnitine
--Vitamin D (incorporated in the phospholipid membranes and prevents lipid peroxidation)
--Avoid toxins: wheat/gluten/grains/x-s-fruit-fructose/legumes/lectins (which GLOM on and/or generate mitochrondria-auto-antibodies), heavy metals (lead, mercury, aluminum, etc), pesticides, synthetic hormones/horsey-hormones/progestins, drugs/pharmaceuticals (eg, statins for MANY), bisphenol, plastics, acrylate (used in enteric-coating of pharmaceuticals, e.g. Costco 'high potency' fish oil)

Statins Can Make You Dumb...

Study Questions Evidence Behind Heart Therapies

Ron Winslow from the WSJ just wrote on 2/24/09 about a new JAMA study finding that "about half the medical recommendations for heart patients have limited scientific backing..."

"Heart disease is among the most studied illnesses in all of medicine, yet just 11% of more than 2,700 recommendations approved by cardiologists for treating heart patients are supported by high-quality scientific testing, according to new research..."

Experts Disagree
But such examples are the exception. For a variety of other conditions, treatment recommendations rely largely on non-randomized studies or expert opinion. For instance, it's unclear at what point patients who suffer excess bleeding during a heart procedure should get a blood transfusion, Dr. Tricoci says. And debate rages among cardiologists over two new tools for assessing a patient's long-term risk of a heart attack. When does a blood test for a marker called C-reactive protein aid in making such a prediction? How about a scan to check for calcium buildup in a patient's arteries? Mounting evidence supports each test, but more data are needed to determine how they might best be used, Dr. Tricoci says.

Harlan Krumholz, a cardiologist at Yale University School of Medicine, says doctors should disclose to patients the strength of the evidence behind the care they recommend. "Treatment decisions are often made very dogmatically even when the level of evidence isn't very strong," he says.

One reason for the lack of stronger evidence is that the large "megatrials" that have dominated cardiovascular research in the past decade were sponsored by drug and device companies. While those studies provide an important source of information, they are typically designed primarily to win approval for a treatment or to widen the market for a therapy already on the market, and not to guide treatment decisions, according to the JAMA study.

Limitations of Studies
Clinical studies also typically exclude patients with complicated illness, which can limit the ability of doctors to apply findings to many of their patients. For instance, many heart patients also suffer from kidney disease. But contrast agents typically given to patients undergoing a diagnostic X-ray called cardiac catheterization can be harmful to kidneys.

Dr. Tricoci says he and his colleagues also observed that guideline writers are picked for their expertise in the field -- but they are also often those who consult regularly with industry. Such possible conflict of interest raises the potential to introduce bias into the guidelines, undermining their credibility."

New PNAS Article: Statins Can Make You Dumb . . .

Along with the above commentary, yet another recently published journal article reports how statin therapy can affect and reduce brain neurotransmitter function. For those susceptible (eg, mitochondrial dysfunction, genetically present mitochrondrial variants, etc), those on excessively high dose statins or perhaps any dose can experience frequently reported statin side effects: 'brain fog', short-term memory loss, erectile dysfunction, muscle aches, tingling/burning in the extremities, peripheral neuropathy, etc.
Cholesterol-reducing Drugs May Lessen Brain Function, Says Researcher

The Testosterone Guide to Happiness

Admittedly I don't always read T-nation.com for its...uuumm...articles, but some of the pieces at T-nation are exceptionally informative. I have to share the next one. I'm always looking for ways to bliss out...this is a great guide from a happy guy's perspective. Do we use 'T' at TrackYourPlaque.com? All hormone optimization to 'youthful' levels generates exceptional plaque reduction and inflammation control, not excluding use of the 'T' or other hormones like thyroid or calcidiol (vitamin D). If age-related changes or damage from wheat/nutritional deficiences/etc prevents 'youthful levels' of hormones, then supplementation provides the bridge for optimal health, longevity and vitality. The 'T' has a role in plaque reversal and control of the toxic, accelerant of inflammation and tissue damage, Lp(a) (lipoprotein little 'a') carried by 17-25% of the population and responsible for ~99% of premature heart and stroke events (age less than 50 for men; 60, females).
TYP Report: Value of Testosterone to Treat Lipoprotein Disorders and Plaque


Dr. Davis made some recent comments about his deep experiences with Vitamin D, this amazing pro-hormone/vitamin/omnipotent-health-regulator.

Vitamin D is a pro-hormone and by controlling blood concentrations of vitamin D, Dr. Davis has witnessed not only accelerated coronary atherosclerosis stabilization and regression, but indeed a myriad of other 'side benefits' like amelioration of claustrophobia, reduction of non-cardiac sternum/chest pain, reversal of aortic valvular disease and even elimination of an autoimmune condition in males that causes debilitating spinal degeneration and chronic pain called alkylosing spondylitis.
Dr. Davis' Unique Vitamin D Observations




Dr. Davis has discussed in the past the benefits of optimism, otherwise known at TrackYourPlaque.com affectionately as Vitamin 'O'. Happiness is not necessarily inborn but can be specifically cultivated. Here is a brief outline from TC (T-Nation.com writer) on how to increase happiness and a little Vitamin 'O'...enjoy!


ATOMIC DOG: The Testosterone Guide to Happiness By TC

Happiness Barrier #1: Complexity
Solution: Simplify

Happiness Barrier #2: A Breakneck Pace
Solution: Take a Pause

Happiness Barrier #3: Negativity
Solution: Let Go

Happiness Barrier #4: Suppressing Sadness
Solution: Feel the Real

Happiness Barrier #5: Navel-Gazing
Solution: Connect With Others



His methods to further increase happiness:

1. Do Dangerous Things. "Dangerous" is a relative term.
2. Do a Friend Dump
3. Find the Female Goose to Your Maverick (and gals…vice versa…find your male Maverick...or equivalent MILF gal-pals)
4. Experience Debauchery
5. Own Less Sh*t, Eat Less Sh*t
6. Look Inside People
7. Make Your Body a Piece of Art

Animal Pharm Science: Vitamin A Deficiency Increases Marbling

Do you want marbling in your meat? I mean, fat-infiltration of your meat-muscles...biceps, triceps, quads and gluts.

M-A-X-I-M-A-L gluteus maximus is what I'm going for! Maximization with functional exercises like squatting and digging volleyball-style which is oh-so-nice...

Not... marbled...meat!!

Looking at journals of animal farm science, studies for increasing USDA Grades of beef and Marbling Scores (MS) have yielded some interesting perspectives regarding vitamin A and its role in controlling obesity. Do Americans get enough vitamin A? The beef industry has figured out that better grades and thus higher market value can be achieved by restricting vitamin A in the food fed to commercial cows. In fact, by depleting liver stores and restricting the content in food, the grade of meat and percentage of intramuscular (IM) fat increase quite substantially. Better yield for livestock owners. Higher levels of blood glucose (BG) are also associated with lower vitamin A status and higher marbling.

HHHhhmmm... why??

Is the livestock which is raised commercially on grains clinically obese, diabetic, inflamed, cancerous (well, unlikely...they're slaughtered too young), high in MUFA, low in saturated fats, vitamin A and vitamin D deficient? With vast desaturase deficiencies?

Livestock owners may be purposefully inducing vitamin A deficiency in order produce higher USDA grade meat for the market. Should we be consuming this kind of low-quality protein?

Humans are actually not that different biochemically and physiologically from our bovine cousins. At one time, bovine insulin was used in Type 1 diabetes mellitus treatment and management. Until human recombinant insulin was developed, pork and beef-derived products were it. Porcine (pork) insulin actually produces less skin irritation and injection site adverse effects like (lipodystrophy, allergic reactions) than bovine, yet bovine filled the needs of many Type 1 diabetes individuals for decades.

One the most curious observations is how cows become very lean (and thus less profitable for ranchers) during spring and summer. This is theorized to be secondary to the increased vitamin A intake from pasturing and eating grass. Vitamin D and increased sunshine probably can be attributed to this relevation as well.

The last set of researchers link how our steroid nuclear receptors are all interrelated in controlling adiposity and the creation of fat cells (adipocytes). They propose a "model of vitamins A and D as suppressors on adipocyte development through retinoid/thyroid/vitamin D/fatty acid-activated/peroxisomal proliferator-activated receptor's subfamily." PPARs have been discussed here before and their crucial role in attenuating chronic and acute diseases including CAD and cancer: Happy Cows...etc.


Who might be vitamin A deficient?
--those who don't consume a lot of wild seafood/grassfed meat (like me but I've discovered... Whole Wallet now)
--those with Hashimoto's hypothyroidism -- Hashimoto's (vitamin A supplementation improves iodine efficacy; hypothyroidism=first sign of vitamin A deficiency in chicks)
--Oprah Winfrey
--Steve Jobs
--those with other autoimmune diseases: Grave's, RA, SLE, Sjogrens, multiple sclerosis, NASH, primary biliary cirrhosis, (??!) CAD, etc
--those with cancer -- see HERE and HERE and HERE--chronically ill
--those with infections or high CRP -- see HERE, HERE and HERE
--children less than age 4 and women -- see HERE too
--those who eat 'low fat'
--those with skin conditions (again, autoimmune origin and wheat-triggered): eczema, rosacea, skin cancer, poor wound healing, atopic dermatitis, psoriasis, dermatitis herpetiformis, porphyria cutaneous tarda
--diabetic-induced rats fed vitamin A deficient lab chow
--those with gluten enteropathy, (known v. unknown) wheat/casein allergies, 'leaky gut' and a poor intestinal barrier which prevent absorption of fat and fat-soluble vitamins
--those without a gallbladder who may not produce sufficient digestive enzymes to absorb fat and fat-soluble vitamins
--those who take Orlistat/Xenical or OTC Alli (weight loss pills which block fat and thus fat-soluble vitamins ADEK1 K2)
--those on antiseizure drugs (valproic acid, carbamezepine, phenytoin which increase metabolism/elimination of vitamin A)
--vegans
--those who have had gastric bypass which unnaturally cuts out a great portion of our most important absorptive surface area for fat and nutrients, the duodenum
--Inuit children with frequent lower respiratory tract infections and otitis media (who are probably no longer consuming their traditional H-G-fish Paleo diets but the S.A.D. grain-based one like Americans)
--third world countries where night-vision blindness is prevalent



What dose of Vitamin A is sufficient?

Like Vitamin D, we need adequate amounts Vitamin A for optimal health -- the desired amount is dependent on various factors: inflammation, growth, reproductive state, hormone state, etc. Vitamin A is not the same as beta-carotene, which is the precursor of Vitamin A. Beta-carotene is the common form found in multi-vitamins.

The current RDA for Vitamin A is 5,000 to 10,000 IU daily (take in AM -- may cause insomnia). Converting from RE mcg to IU see HERE.

Here are other benefits of Vitamin A discussed here: Synergy of Vitamin D and Its Co-factor Vitamin A
Consideration for Vitamin A supplementation is necessary if diet (wild seafood, grassfed meat, organ meats) are insufficient to meet daily requirements.

Ck out Vitamin A...for your healthwise b-o-t-t-o-m . . . line. I'll be watching it for you. *wink*

Hey Gibby -- this post is per your request!

CLICK ON CITATION TO VIEW (below)
"...long vitamin A restriction (LR) specifically increased fat deposition in the i.m. depot, without promoting an increase in the overall fatness of the animal. We conclude that feeding low-vitamin A diets may be a feasible and economical strategy to affect the site of fat deposition within the beef carcass. Pyatt and Berger (2005) hypothesized that the observed seasonal decline in carcass grade during the fall may be associated with previous high-vitamin A intake during spring and summer. Additionally, typical feedlot diets are formulated to provide 2 to 3 times NRC (1996) vitamin A recommendations (Galyean and Gleghorn, 2002). Thus, feedlot cattle in the United States are fed vitamin A in excess of their requirements. Results of
this experiment provide evidence that the vitamin A level of the diet affects the site of fat deposition in feedlot cattle.

We recently reported that feeding low-vitamin A diets to beef steers appears to increase adipocyte differentiation in the i.m. depot without affecting s.c. adipocytes. This was accompanied by numerical in- creases in marbling scores and USDA carcass quality grades, with no effects on backfat deposition and USDA yield grades (YG; Gorocica-Buenfil et al., 2007). Marbling scores also were increased when low-vitamin A diets were fed to Japanese Black cattle (Adachi et al., 1999). The duration of vitamin A restriction required to improve i.m. fat deposition remains unknown. It is likely that to affect the vitamin A status of the animal, hepatic vitamin A stores need to be depleted. However, research in this area is negligible.

The effect of feeding low-vitamin A diets on beef fatty acid composition remains unclear. The enzymatic activity of stearoyl coA desaturase (SCD), required for the endogenous synthesis of CLA in ruminants, may be reduced by retinol (Alam and Alam, 1985). However, a numerical trend (P > 0.10) was observed in marbling score and the percentage of carcasses grading USDA Choice or above (from 28% in control to 50% in LR steers). If this effect were real, it would be economically important because most formulas used in the market to determine carcass value include a premium for
carcasses ≥ Cho (USDA Agricultural Marketing Service, 2006). The numerical increase in the percentage of highly marbled carcasses is in agreement with our previous experiment (Gorocica-Buenfil et al., 2007) where we reported a 7% increase in the marbling scores when low-vitamin A diets were fed to Angus-based steers."Effect of dietary vitamin A restriction on marbling and conjugated linoleic acid content in Holstein steers. (PDF) Loerch SC et al. J Anim Sci. 2007 Sep;85(9):2243-55.Relationship between serum biochemical values and marbling scores in Japanese Black steers. Ohwada K et al. J Vet Med Sci. 1999 Aug;61(8):961-4.



"Slight changes in the fatty acid profile of s.c. fat of the steers were detected. A greater proportion of MUFA (LOW = 41.7 vs. HIGH = 39.9%, P = 0.03) and fewer SFA (LOW = 47.1 vs. 48.7, P = 0.03) were observed in vitamin A-restricted steers. This suggests that vitamin A restriction may affect the activity of desaturase enzyme (desaturase activity index, LOW = 46.9 vs. HIGH = 44.9, P = 0.01)."Effect of vitamin A restriction on carcass characteristics and immune status of beef steers. Loerch SC et al. J Anim Sci. 2008 Jul;86(7):1609-16.


"It is well documented that grain feeding stimulates adipogenesis in beef cattle, whereas pasture feeding depresses the development of adipose tissues, including intramuscular (i.m.) adipose tissue. Additionally, production practices that depress adipocyte differentiation also limit the synthesis of monounsaturated fatty acids (MUFA). Marbling scores and MUFA increase in parallel, indicating that stearoyl-CoA desaturase (SCD) gene expression is closely associated with and(or) necessary for differentiation of marbling adipocytes. Similarly, marbling scores and fatty acid indices of SCD activity are depressed in response to dietary vitamin A restriction. In bovine preadipocytes, vitamins A and D both decrease glycerol-3-phosphate dehydrogenase (GPDH) activity, an index of adipocyte differentiation..."Cellular regulation of bovine intramuscular adipose tissue development and composition. Sawyer JE et al. J Anim Sci. 2008 Nov 7.



"The study aimed to systematically examine the effects of fat soluble vitamins and their analogs on terminal differentiation of adipocytes on the cellular and molecular aspects. It is well known that fat soluble vitamins especially vitamins A and D inhibit the differentiation of adipocytes in cultured cells. Furthermore, it has been revealed that the low level of dietary fat soluble vitamins, especially vitamin A and carotenoid actively stimulate the development of adipose tissue, namely bovine marbling in vivo. We have shown that the expression of retinoic acid receptor (RAR) alpha and gamma, retinoid X receptor (RXR) alpha and beta, and vitamin D receptor (VDR) mRNA were abundant in rat adipose tissue and 3T3-L1 cells. The autoregulated amplification and reduction of RAR, RXR and VDR mRNA by their own ligands, were observed in 3T3-L1 cells. Finally, we proposed the model of vitamins A and D as suppressors on adipocyte development through retinoid/thyroid/vitamin D/fatty acid-activated/peroxisomal proliferator-activated receptor's subfamily."
The possibility of active form of vitamins A and D as suppressors on adipocyte development via ligand-dependent transcriptional regulators. Sugimoto E et al. Int J Obes Relat Metab Disord. 1996 Mar;20 Suppl 3:S52-7. Review.

Paleo is...SHWINGTASTIC

Why Do I LOVE-LOVE-LOVE Paleo?


Let me give kudos to the some of the originators of Paleo before it became so haawwwwwtttt.....!!


First...RobbWolf.com and Nicki with her stunning 6-pack-abs, co-conspirators in creation of the best gym on earth... NorCal Strength & Conditioning -- Crossfit H-E-A-V-E-N (diablocrossfit.com is SECOND to HEAVEN...being the devils that we are...*haaaa ah*). NorCal is where one can challenge and befuddle the abs, core, shoulder and arms by trying to do wall-balls against a thin 6" rail engineered by Nicki and her favorite helicoptor metal company :) *wink* You guys R-O-C-K !

Their gym was named one of the top 30 in the U.S. according to Men's Health, and featured in my...ummmm... favorite 'journal' Fitness Rx for MEN. Robb and Art DeVany discuss EvFit here in 2005 CLICK HERE.

This post is about aesthetics... Robb discusses Performance-based Aesthetics much MUCH better than moi... CLICK HERE.

Now, Robb, dear . . . still waiting for your soon-to-be-best-selling seminal B O O K...!


Now going clockwise, Son Of Grok (SOG), the Paleo protege and recent transformer. Great blog, food p*rn and insightful thoughts and experiences. Such impressive aesthetics! So fast...so furious... We share common movie interests...like '300' (aahhaa) and his '300' workout (which sounds like a CF filthy 50 or Girls Gone Bad...but 10x worse).


The original Grok, Mark Sisson, King of Bloggers at Mark's Daily Apple and all things Paleo. His motto: 'Serving up health and fitness insights (daily, of course) with a side of irreverence.' I adore (!!) irreverence . . . Mr. Sisson soon will publish his Primal Blueprint which will delight all readers I'm certain and will provide a foundation for optimal longevity and health for all of America. We sure can use it, right? Yet again... behind every strong blogger, there stands an even... hotter partner.


Keith Norris of Theory to Practice engages high level thinking with low level basics. Need I say more? Excellent food, friendly advice, and friggin good workouts! He's got the best quotes too :) and best appreciation for art/literature. Mr. Norris' wife is a model and eats/lives/breathes and also shares ultimate Paleo aesthetics.



How does Paleo create superior aesthetics?

(1) optimal DNA gene expression via suppression of obesity genes, lifespan-shorteners and stress-genes

(2) symmetry achievement by diet/exercise/IF/relaxation as muscles, skeletal structure and ligaments align to optimal configurations

(3) banging hot skin, hair, nails and secondary sex characteristics by hormone balancing (hGH, T, E, DHEA, thyroid, leptin, adiponectin, etc) and insulin normalization (and some EPA+DHA, vitamin ADEK supplementation)


Paleo is...shwingtastic...wow...and so can you be shwinging-fantastic *winky*