Sunday, February 28, 2010

Auto-Tuning Lp(a): Value of Low Carb, High Sat Fat


I've got a big tolerance for stupidity. Even supersized-stupidity. Mostly this is because I am somewhat a bit of ding-dong myself. Luckily... my husband has not divorced me yet after realizing for the millionth time that I'm a complete retardo (and too late, the genes have been dispersed to our offspring *haa*). Recently I put my cellphone through the wash. Seriously.


The stupidity over saturated fat nonsense and low cholesterol diets *sigh* are over the top lately indeed and require a rant. Some cardiologists appear to fear the 'large buoyant LDL' created by saturated fat. I don't get this. Don't our cells possess the biochem to burn our b*tt PHAT? Maybe scientists lack this gene??

Conventional docs aim at LDL which is clearly the wrong target. In the primal/ancestral/crossfit world, the aim is focused on dense LDL. Yes -- this is emphasized by Cordain. He was courageous to stop condemning saturated fat. Xfit nutri certs *big smile* reinforced hyperlipidemia.

Here, biochem tiger Peter deciphers the medical literature. The core of atherosclerotic plaque is made up of lipids, mainly glycolated ones and oxidized LDL (oxLDL).

OxLDL is Lp(a)...
* Lipoprotein (a) is oxLDL
* Statins raise oxLDL and Lp(a)


Let me speak freely.

Saturated fat controls Lp(a). (HERE, HERE, Krauss and DELTA)
Low carb controls Lp(a). (HERE and Volek; insulin-Lp(a))

This translates to the control of atherosclerotic plaque and regression.

It doesn't matter what level of Lp(a) one has (remember, Hecht showed that disease is associated with levels of 2 to 200 mg/dl) -- Lp(a)/oxLDL is like a 'spark' when lit. What lights up Lp(a)??! OMG. Saturated Fat Deficiency and Insulin. Hyperlipidity fixes Lp(a) and regresses plaque -- let Big Pharma chew on that. Are they colluding to keep us 'low sat fat'? It's not difficult.

Again. The only quartile associated with regression in women in ERA was the high saturated fat quartile. Mozzafarian et al. This is what I observe as well in real life.

Niwamae et al analyzed biometrics in 203 patients with peripheral vascular disease using IVUS. Plaque morphology was also analyzed: soft, hard/calficifed and lipid cores.

Should you be scared of intimal flaps? Errr. Yeah. If I had plaque -- I'd prefer 4-digit calcifications with stable hard-cores, than 2-digit FLAPPY soft-core plaque. Plaque rupture has been highly associated with the presence of intimal flaps -- like a poorly treaded Firestone, they are ready to burst with collision with sticky highway rubbish or pounding speeds.

Intimal flaps were only associated with 3 things according to Niwamae (see Fig 3, above):
(1) insulin resistance (read: high carb)
(2) low HDL (read: REALLY dense LDL, low sat fat, high carb)
(3) high total cholesterol (read: denseLDL/apoB/TG, high carb)

What lights up insulin? Carbs.

Read. High carbs KILL.

Carbs cause cancer. Carbs cause cholesterol concerns. Carbs cause PLAQUE.


I like butter. *aah* EAT MORE BUTTER.

Recall, Ai M et al (boy the Japanese scientists ARE SO D*MN SMART) demonstrated that carbs trigger insulin, NOT SATURATED FAT. Previous animal pharm: Insulin and Aging, How Paleo Works

Soft plaque known as fatty streaks even develop in young hearts (Peter has a picture) and don't calcify unless oxidation occurs. EBT studies show that 95% of diabetics have calcified plaque, the other 5% probably have soft plaque which are vulnerable to stenosis. Why? Individuals withi diabetes are damaged/oxidized from carbs and insulin. How do you prevent oxidation? Eat some saturated fat d*mn it (ghee, butter, animal PHAT, coconut products, lard, beef, seafood, organ meats, schmaltz, etc) and keep your insulin low with a carb-appropriate diet (minimal fruit, no grains, no oats, no legumes, no soy) and lifestyles that are aligned to your evolutionary genetics. Maintain an intake of very low n-6 oils. Anything > 2-4% of the diet is excessive because it is associated with raising insulin resistance, CAD, cancer rates and inflammation. Walter Willet at Harvard and certain heart programs advise 40% fat with only *gasp* 8% sat fat and 15+% n-6 oils. Heart stopping and insane, isn't it?

Get In Line


There are a lot ding-dongs out there. In academia, the USDA, the ADA, the AHA and conventional cardiac programs (Dean Ornish)... T. Colin Campbell *haa* GO PALEO KING 'the stupidest think I've read'.

Take It Off

One thing I hate about the radio is the overuse of auto-tuning, a software technology employed that takes normal voices and 'tunes' up to desired levels, usually 'pitch perfect'.

The imperfect sounds better to me -- texture, depth, emotions shine through.

Naked. It ROCKS. Naked is true. *HA HAA*

Blah Blah Blah

How many times do we hear about low saturated fat diets? Too often.

Do they work? Hardly. Heart disease is still #1 in killing Americans. Low fat isn't working. Americans are SICKER, FATTER, and MORE TIRED than before 'low saturated fat'.

This Love...

For low fat is pervasive. People feel guilty and 'not healthy' if they fail to follow this advice from their esteemed cardiologist or doctor... I nearly choke when I see HDLs as low as 30's or 40's and people tell me they cut out egg yolks and fat. This is reflected in a heart-deadening drop from HDL of fantastic 60's 70's earlier. Their LDL's are subsequently auto-tuned with a statin to TESTOSTERONE-NUMBING levels of 40's to 50's.


Then they tell me they are using more canola oil, olive oil and wholeheartdisease grains and oatmeal, and I wanna CRINGE and puke out loud. No wonder their numbers S*CK. Initiation and promotion of atherosclerosis and other inflammatory conditions (cancer, autoimmune, migraines, etc) are indeed inevitable.

You're Freaking Me Out

No. Unlike the current management of CAD (coronary artery disease) and the 'tuning' of LDL-cholesterol where Big-Pharma-sponsored heart disease management guidelines (NCEPIII) advise LDL < 70-100 mg/dl for for those with CAD or heart disease equivalents (EBT calcifications, diabetes, aneurysm, peripheral vascular disease, etc)... or other programs that endorse LDL of 60 or below, in contrast, low carb high sat fat evolutionary diets WORK. Small dense LDL are obliterated to zero or near zero. These individuals have heart scans of zero calcifications and definitive regression over time. Show me zero dense LDL and I will show you reversal. Here to be redundant are those succeeding: My Paleo Peeps.

Pushing the LDL below natural, naked, endogenous baselines with Big Pharma drugs (statins, zetia, vytorin, etc) miserably fail from my extensive observations, EBT statin trials (10 out of 12 show progression w/statins) and new ones like ARBITER-6 (vitamin B3 beats the cr*p out of zetia). EBT calcifications continue at unacceptable rates (20-50+%), heart attacks and re-stenosis of stents and bypasses still occur, and disability from lower extremities, kidneys, and failed hearts flagrantly progress despite *cough cough* 'life-saving' statins.


Archaic guidelines need to go extinct. Now.


Kesha's one of my favorite animals right now... The grrrrl cracks me up: Rolling Stone interview. If there's auto-tune, I can't tell... She sounds perfectly IMPERFECT.

While You Were Sleeping

Stuff is happening. Pro-active work in the blogsphere, media outlets, movies like Fathead, books like BSS, Primal Blueprint, and 6-Week Cure and... how 'bout infomercials with some haaaawwt Paleo peeps? We need some. Cordain and Wolf are putting together continuing education for docs -- he said they need a pharmaco person... so might fill in and express my st*pidity *haa*.

Boots And Boys

Not only are Crossfit boys and grrrrls ridiculously super HAAWWT but also require no auto-tuning w/drugs as optimal health falls naturally into place. Avoiding neolithic toxins (legumes, graines, dairy, refined n-6 oils, statins/drugs glyphosate herbicides, etc), eating whole foods, and taking nutraceuticals maximize our evolutionary heritage (omega-3, digestive enzymes, probiotics, vitamin D, insulin sensitizers, etc). These endogenously 'auto-tune' employing our inherent software, e.g. DNA and nutrigenomics.

Ultimately, Crossfit + Paleo (Robb Wolf + Nicki Violetti) and our ancient/primal/Protein-Power blogosphere are where I find unprecedented reversal stories. Mr. Billy E did so with only diet (Evo/Paleo low carb, high sat fat) and vitamin D!

A Bad Girl's Lament

What I've noticed is that the athletic field often 'get it' before the medical. A great example is the use of omega-3 fish oil by Dara Torres and other athletes. Ultimately performance trumps lipid panels. To me, results are strikingly self-evident with low abdominal obesity, X-image '300' buff xfit-trained warriors, NBA stars, cycling and Tour de France competitors, and Olympic stars like Apolo Ohno. Slowly people will figure it out and stop listening to their low-fat, conventional, Big Pharma-bribed, Koolaid-drinking doctors.
--Apolo Ohno, 4X Olympic Speedskater (NYT: coconut oil, eggs, low carb, appears grain-free (except rice prior to events))
--Christian Vande Velde, Tour de France (MH: Winning Without Wheat)
--Runner's World, Aug 2004, Should You Be Eating Like A Caveman?
--Men's Health: How the Low Fat Craze is Making Us Fat
--Beijing Olympic gluten-free foraging, runner Amy Yoder Begley

Tuesday, February 16, 2010

Dietary Carb 20-40 grams/day To Control BG

BG = Battlestar Galactica... *ha* j/k

BG = Blood Glucose

I loathe giving a limit to dietary carbohydrate intake but I get a lot questions regarding this.

Ideal Carb Intake for the Metabolically Challenged

20 to 40 grams daily
(with carb cycling 40 - 80 g on rare days -- to replenish glycogen after full depletion)

Why? This works, for broken metabolism.

Broken Metabolism

Carb intake for those with 'broken metabolism' like myself who used to carry 50 lbs of fat previously require meticulous and vigilant control of dietary carbohydrates and maintenance of basal metabolic rates via exercise. For us, carbs, fructose and omega-6 signal 'INSTANT' hibernation (fat gain, impaired immunity, sdLDL, low HDLs, autoimmunity, poor gut-brain axis). INFLAMMATION.


It is the Winterization v. Over-Summerization concept where our bodies are furtively storing for the winter that never comes. The adipose organ is damaged and continues to believe it is fulminant fat-storage time, not fat-burning time. Prior nephropal:
Phat Fat Accumulation versus Mobilization

20 to 40 grams per day is an amount that helps to control insulin, BG (blood glucose) and improves body fat recompositon. Yes -- improves sdLDL (small dense LDL) and Lp(a) as well and allows subcutaneous and visceral fat regression, regression of vascular calcifications (e.g. plaque, hypertension), prevention of senility (Alzheimer's also known as Type 3.0 Diabetes), cancer protection and overall optimal health and lifespan (and an X-image *wink*). Carb cycling (+resistance training/exercise) prevents long-term reduction in basal metabolism as well as maintains enough subcutaneous fat. Under the skin fat, subcutaneous, is brown GLORIOUS fat which provides the youthful, X-image, in all the right places. Without brown fat we can get excessively saggy, droopy, wrinkly skin folds. (also that just takes TIME to tighten up after dramatic weight loss... like 18-24 months... sorry) Intermittent ketosis (intermittent fasting and ketogenic diets) improve insulin sensitivity and insulin secretion. Ketosis is like a cheat... simulates a negative energy balance (as carbs are taken out of the picture). We are built to be ketotic and use the prime fuel of our mammalian systems: fatty acids and ketones. Newbornes are ketotic the first 2 weeks of life as the maternal colostrum and milk are coming in.

What the h*ll are carbs?
Anything your tongue perceives as sweet (including fruit) or starchy.

Use for help. Do note their reported servings sizes which are often not typical. Take into account in the calculations. is good as well I've heard.

Examples of 15 grams of carbs:
--1/3 cup oat bran (i.e. 2 bites and I have a big MOUTH; this raises my BG in 5-10min to 150-180 g/dl. No SH*T)
--palm-size orange, apple, banana (the worst due to starchiness), grapes, CUTEYS
--1/3 cup brown or white rice (doesn't matter they ALL raise BG)
--candy -- 1 bite
--ice cream 1/2 cup (not as huge a BG rise due to fat buffering effect from full cream)
--1 cup of milk (doesn't matter if low fat or full fat)

--1/3 to 1/2 cup juice or reg soda (depends on brand and HFCS content)
--1/3 cup pasta
--1 slice bread (rice bread is worse due to higher density)
--1/2 cup mashed potatoes

BG Mini Curve: Monitoring

Do you have a glucometer? The blood glucose curves for cats are better done than for humans IMHO (see diagram, courtesy of Vetsulin). Consider doing a 'mini curve' examining the effects of dietary carbs and combinations of food and lifestyle effects (exercise, intermittent fasting, STRESS STRESS, sleep deprivation, resistance/weight training, etc). Consider monitoring closely and tightly from 5-15min after food and additionally 30 v. 60 v. 45 v. 60 v. 90 min after food.

Feline 'mini curve'
Remember Ai M's study on carb loading v. fat loading and the insulin effects? Click here: insulin and aging. The same curve can be superimposed for dietary carbohydrates -- blood glucose rises within 5-10 minutes of a carb load. If I consume (depending on the time of the month and how much exercise I'm doing), my sugars can climb and peak to 180 mg/dl easily with 1 cup of rice in less than 10 minutes. And... I generally feel cr*ppy for the rest of the day (flushed, fast heart rate, hypersensitive).

When a diabetic patient has a hypoglycemic reaction (low glucose < 60 mg/dl; signs and symptoms include sweating, hot flash, tremor/shakes, fast heart rate, irritability, anxiety, palpitations, hunger, tunneling vision, headache/migraine), a glucose source will generally start to raise the blood glucoses within 5 to 10 minutes. Usually only medications lower the glucose so significantly (insulin or an oral drug, e.g. glyburide, glipizide, Amaryl). Exercise + medications is a potent combination. Exercise for some individuals is equivalent to 10 to 20 units of insulin.

What are goal glucoses? Why are they elevated in the first place? Adrenal insufficiency (which is associated with reactive hypoglycemia)? Untreated, undiagnosed hypothyroidism? Excessive carb intake? Lack of resistance training? Sarcopenia? Lack of exercise? Sleep deprivation? Excessive mental stress?

Fix these first then consider focusing on BG.

Here is the relationship between HgbA1c and average glucoses (click HERE) -- written by a fan of Dr. Bernstein's , a patient educator and advocate who has an A1c of 4.7% and is a Type 1 diabetes patient himself and medical physician.

Goals stated previously (HERE): HgbA1c < 5.0%

Glucoses > 140 mg/dl are associated with AGEs RAGEs and other glycosylation products and damage, including diabetic complications (kidney, eyes, nerves, brain, blood vessels, erectile dysfunction, hormone dysregulation, endocrine glands, etc).

We are not M&Ms. Don't sugar-coat yourselves.

Ultimate goal for health: as normal as possible (flat curve at 97 mg/dl or lower)

Success Stories

See prior paleo CAC success stories achieved with low carb, high sat fat Paleo or 'Dai-leo'(update Jimmy Moore and Scott have zero plaque):
My Paleo Peeps With High HDLs

Mr. Billy E is my HERO! Reversed CHF, chronic kidney disease, Type 2 Diabetes (T2D), dyslipidemia (high TG, low HDLs) and hypertension on low carb, high sat fat Paleo. Click HERE and HERE Look what happened on the way back to the cave.

Control of BG, Insulin, and Leptin

Stephan has articulately enlightened on leptin ( still I just don't completely get it yet... coz I'm a ding-dong). Leptin appears to be the long-term messenger for energy balance, reproduction and control of hunger and certain behaviors...
Wholehealthsource: Leptin
Excellently expressed and illuminating insulin resources which have helped me in my understandingof the hormone cascades are below. Though I have a CDE, certified diabetes educator 'credential', these broadened my knowledge by a ~milllion-fold... because... I admit *blechVOMIT* I used to be a card-carrying ADA member.
-Dr. Guyenet (Stephan) at WholeHealthSource: Body Set Point series, Paleo Diet series, Low carb diets, Fatty Liver, Visceral Fat, Omega-6/Fructose, Butyrate, etc

-Drs. Mary and Mike Eades: ProteinPower books
-Dr. Harris at PāNu:
How to lose weight and Get Started
-Dr. McGuff of Body By Science:
Internal Starvation and Especially for Women

Robert McLeod's thoughts on insulin and other hormones are what I have been thinking about for a while and what I have found personally to work for lifestyles. I would agree and concur on all his 13 points.

Entropy Production:
Hormone posts by Robert McLeod (I consolidated)

1. Very long and very slow exercise (4+ hrs), typically hiking or cycling in my case. This is a far cry from the type of anaerobic-limit cardio exercise one typically sees recommended, for example, by the American Heart Association. There is a yawning gulf between walking and jogging. I personally approve of anaerobic exercise, such as sprint intervals or plyometrics.

2. Consistently eat carbohydrates at a low enough level that the brain (which prefers glucose over ketones) consumes the entirety of carbohydrates that you eat, leaving the body to burn ketones. This is a slow process.

3. Periodically fast for an extended period of time so that your basal metabolism burns through your glycogen reserve and then begins to mobilize fat. This is not a calorie reduction method, rather you are simply not eating three times a day (on average), and as such having more extremely calories negative and calorie positive periods.

4. Get adequate sleep. GH production spikes during sleep. Try not to eat before bedtime.

5. Fast occasionally, for relatively short durations.

6. Conduct intense exercise. Don't eat before or during your exercise.

7. Control appetite hormones like gherlin by eating regular, satiating meals. By satiating I mean protein, fat, and fibre. Try to avoid snacking.

8. Restrict fructose and alcohol consumption to reasonable levels, day-to-day. 20 g/day of both combined would be a very healthful level, 50 g/day is I think an upper bound for people with healthy livers.

9. Eliminate industrial, refined oils, particularly refined polyunsaturates such as soy and canola oil. Go for fresh and high quality fats, in particular clarified butter, extra-virgin coconut oil, extra-virgin olive oil, and the fats from animals fed their native diet. Unstable oils should be stored in the refrigerator or freezer to prevent them from going rancid, e.g. Omega-3 fish oil capsules. Most industrial oils are deodorized to prevent you from smelling when they go bad.

10. Eat more than just muscle meat from an animal. Have you eaten liver pate or roasted heart lately? Bone broth?

11. Fast occasionally for approximately 24-hours to give your liver a break and restore insulin sensitivity. Many religious groups noted for their good health (i.e. Seventh-day Adventists, Mormons, and the Greek-Orthodox of Crete and Corfu) regularly fast — is the the shared common trait. Fasting and starving are not the same thing, don't conflate the two.

12. Go on elimination dietary trials of the common food allergies: wheat (including barley and rye), cow dairy, legumes, especially soy and peanuts, tree nuts, eggs, fish, and shellfish. Test assays may be insufficient to recognize many of the idiopathic problems (i.e. autoimmunity, neurological disorders) that these types of food may induce. It took me six months wheat-free to get better.

13. Supplement with Vitamin D, on the order of 1000 IU/12 kg of body mass per day. Consider that the recommended doses for infants are 400 IU/day, so if you mass ten-times that of an infant, you need ten-times as much vitamin D; recommended adult doses are a joke. Also consider that you produce about 10,000 IU/ 30 minutes in full-sun. Vitamin D is not a vitamin, it is the precursor material to most of the steroid hormones in your body. When the endocrine (hormone) system has adequate signaling compounds, the whole body works better.

Leptin and Leptin Resistance

Dr. A's post is eye-opening.
Mastering Leptin book report (but note her '????'s where I think she politely says wtf)

Factors that shut our brain off to messages like leptin and therefore raise leptin resistance and impair transport of leptin across the blood-brain-barrier are non-paleo foods and lifestyles:
excessive fructose
--maternal magnesium deficiency (epigenetic changes in rats)
dairy fats (?unfermented A1 casein)
lectins (grains, oats, corn, legumes, soy, peanuts) -- (unsoaked seeds and nuts too -- these are fattening if excessive!)
--screwed up
gut-brain axis
--lack of sustained 2-4 hr exercise and/or resistance training
--factors that induce hypertriglyceridemia: omega-3 deficiency, excessive carbohydrate diets, sedentary lifestyle, synthetic hormones (progestins, endocrine disruptors, Teflon, pesticides, bisphenol, etc), estrogen/vitaminD/testosterone/DHEA deficiencies
--deficiency of saturated fatty acids (short-
medium- long-chain)
excess omega-6 and/or deficiency of omega-3
--high cortisol (stress, endurance train/events, poor sleep)
--starvation (excessive intermittent fasting, hypocaloric diets)

--gender (females more affected, esp with all factors listed above)
--genetic programming (epigenetic influences -- stressors: drought, famine, protein-restriction)

Saturday, February 6, 2010

Hypertension and the X-Image

From the left: Mechad Brooks (from True Blood), Spanish tennis player Fernando Verdasco and Japanese soccer player Hidetoshi Nakata.

How is the X-Image and Hypertension Related?

[This is not a stretch... *wild wink*]

For men, this is the balanced, broad shoulders, narrow hips image. For women, strong symmetrical shoulders, narrow waist, wide child-bearing hips, long gams. The X-look was coined by Prof DeVany. Evolutionarily, secondary sex traits are associated with high fertility. For both genders, a narrow waist signifies high hormones -- testosterone (not hair-losing-DHT), estrogen, progesterone, DHEA, pregnenolone, etc. And... Low insulin, low insulin resistance and low inflammation and, thus, high immunity and resistance to lethal infections, the biggest killer of ancestral man besides predators and famine/drought.

Low insulin and low insulin resistance also corresponds (typically) to no visceral fat (intra-abdominal adiposity)... and narrower waists, precisely, the X-image.

Many genetic adaptations derive to push forward genetic material to the next generation and to provide for a stronger immune surveillance and protection system. Peter will soon be discussing the (protective) role of Lp(a) and the evolutionary disadvantages of vegetarianism. Bantu vegetarians not only have higher Lp(a) but also higher blood pressures.

Brain, Neuropeptides, and Hormones

The primary controller of fertility and sexual function is our... BRAIN.

I am not joking. Indeed, the brain is our biggest sex organ.

The pituitary-gonadal axis influence sex hormones and fertility by incorporating multilevel inputs from the intestines/GI, muscles, senses (eyes, ears, mouth/ philematology, smell/ pheromones), fat stores, liver, etc .

Scheider JE discusses the balance of energy and reproduction thoroughly. Two diagrams are from Energy Balance and Reproduction, click for PDF HERE.

Energy Balance and Reproduction
The physiological mechanisms that control energy balance are reciprocally linked to those that control reproduction, and together, these mechanisms optimize reproductive success under fluctuating metabolic conditions. Thus, it is difficult to understand the physiology of energy balance without understanding its link to reproductive success. The metabolic sensory stimuli, hormonal mediators and modulators, and central neuropeptides that control reproduction also influence energy balance. In general, those that increase ingestive behavior inhibit reproductive processes [e.g. excessive carbohydrates], with a few exceptions. Reproductive processes, including the hypothalamic–pituitary–gonadal (HPG) system and the mechanisms that control sex behavior are most proximally sensitive to the availability of oxidizable metabolic fuels. The role of hormones, such as insulin and leptin, are not understood, but there are two possible ways they might control food intake and reproduction. They either mediate the effects of energy metabolism on reproduction or they modulate the availability of metabolic fuels in the brain or periphery.

This review examines the neural pathways from fuel detectors
to the central effector system emphasizing the following points:

0 First, metabolic stimuli can directly influence the effector systems independently from the hormones that bind to these central effector systems. For example, in some cases, excess energy storage in adipose tissue causes deficits in the pool of oxidizable fuels available for the reproductive system. [Recall, insulin stores/locks in fat. We need 'some' insulin for muscle growth, but really not much. Hard-gainers have insulin resistance in the liver and elsewhere, I strongly suspect.] Thus, in such cases, reproduction is inhibited despite a high body fat content and high plasma concentrations of hormones that are thought to stimulate reproductive processes. The deficit in fuels [fatty acid fuel deficits caused by carb-pathways turned on] creates a primary sensory stimulus that is inhibitory to the reproductive system, despite high concentrations of hormones, such as insulin and leptin.

o Second, hormones might influence the central effector systems (including gonadotropin-releasing hormone (GnRH) secretion and sex behavior) indirectly by modulating the metabolic stimulus.

o Third, the critical neural circuitry involves extrahypothalamic sites, such as the caudal brain stem, and projections from the brain stem to the forebrain. Catecholamines [adrenaline, stress], neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) are probably involved.

o Fourth, the metabolic stimuli and chemical messengers affect the motivation to engage in ingestive and sex behaviors instead of, or in addition to, affecting the ability to perform these behaviors. Finally, it is important to study these metabolic events and chemical messengers in a wider variety of species under natural or seminatural circumstances.

Insulin and Leptin 101 Basics

For more insulin and leptin 101 basics, please see Dr. A, my soul sister in science *BIG SMILE!*
--Mastering Leptin book report (but note her '????'s where I think she politely says wtf)

Stiffness. Caused by Insulin and ROS.

OK sometimes we want stiffness.

Er... But not forever...

Like a rubber tubing left outside to the elements, the vascular system in mammals (and fish) will stiffen and crack if it loses contractility and elasticity from oxidative damage. Rubber is resilient, yielding and flexible until it starts to break down from damaging factors such as UV, heat, cold, salt, oxidation, radiation, etc. In biologic systems, unlike rubber, there is respite and forgiving repair. Damage only occurs when the destructive factors outpace the rate of repair. The coronary arteries are most affected due to narrow relative diameters and high shearing forces as blood is pumped from the heart to the peripheral tissues. The higher the pressure, the more potential damage to the endothelium (lining of blood vessels). As the body tries to heal these tiny 'nicks' in the endothelium, scar tissue and calcifications form. If the immune system is on abnormal 'hyper-overdrive' or if the BP is abnormally high, then the scarring and calcifications can be more extensive, more keloidal, more thick with plaque. Those with Lp(a) (at any level, according to Dr. Harvey Hecht's research) tend to over-scar, it appears when the Lp(a) particles are small and oxidizable. Don't be dense. Saturated fat increases the size of LDL as well as Lp(a) (which is just LDL plus apo(a)), which improves the buoyancy and anti-atherogenic properties of LDL and HDL.

Insulin, Insulin Resistance Raise BP and Coronary Calcifications

High blood pressure is a 'gateway' condition to heavier, harder, stiffer conditions. BP greater than 110/70 is one of the first indicators that something is going on... See prior Nephropal post: Insulin.

BP is reflective of our inflammatory status and health of the endothelium. What causes BP to rise? Well. If you ask a cardiologist or any primary doc, they will tell you that essential hypertension has no known cause. WTF. With going paleo, BP, insulin, and insulin resistance are all lowered. Frasetto et al at UCSF showed this (as well as EVERYONE in the paleo community who was previously ill). Click HERE prior nephopal. With going low carb, Meckling et al has shown that BP, insulin and glucose were all also lowered (click HERE).

In the low-fat arm, of course, this was not the case. Low-fat is killing America by raising and maintaining high insulin levels which make us fat and STIFF.

Dr. Houston has discussed known causes of hypertension: ROS (reactive oxygen species), e.g. inflammation. Nephropal post: Nutrigenomics and Hypertension.

o Blood pressure and fasting plasma glucose rather than metabolic syndrome predict coronary artery calcium progression: the Rancho Bernardo Study.

o Insulin resistance independently predicts the progression of coronary artery calcification.

o Adiponectin, visceral fat, oxidative stress, and early macrovascular disease: the Coronary Artery Risk Development in Young Adults Study.

o Psychological stress, insulin resistance, inflammation and the assessment of heart disease risk. Time for a paradigm shift?

o Relationship of adiposity to subclinical atherosclerosis in obese patients with type 2 diabetes.

What Does NOT Raise Insulin?


Pure unadulterated fat.

I aint talking olive oil honey.

See prior animal pharm: Insulin and Aging -- how low carb, high saturated fat works.

What Raises Insulin?

--Dietary carbohydrates (e.g. oatbran, grains, corn, legumes)
--(protein, mildly)
--Gluten (via both the carb route and the endorphin system)
--Cortisol (stress, sleep deprivation, endurance training, etc)
--Hormone deficiencies (vitamin D, testosterone, estrogen, omega-3 fish flax, thyroid, etc)
--Drugs (steroids, birth control, Crestor/ rosuvastatin, Provera/ progestins, water pills, etc)
--Lack of ketones (MCT oil, coconut oil, periodicity of exercise or fasting)
--Sedentary atrophying lifestyle
(Last X-Image: Kellan Lutz, from Twilight series and 90210)

Dr. T's Winterization (good) v. Over-Summerization (bad)

Diagram from Schneider, modified.