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Hypertension and the X-Image

Posted Feb 06 2010 10:23pm
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?

Fat.

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)
--Fructose
--Omega-6
--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.


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