Monday, January 23, 2012

How to Keep Warm During Winter

I think cold legs are a hazard.

Here's an experiment. (For men only.)

If your weather is cold, then do this. Perform extreme exercise until you feel hot. Then take all of your clothes off. Cool down in the cold temperature for two or three minutes.

Compare how warm your thighs feel with how warm your lower-legs feel? Do you feel colder in your lower-legs?

Then touch your thighs. After touching your thighs, touch your the front of your lower-legs. Then touch the back of your lower-legs.

See the difference in temperature?

The first thing that you will feel is that your lower legs will feel cold. Not your thighs. Your lower legs will feel cold. Yet if you touch them, they don't feel cold. They feel warm. But thighs are in the opposite. If you touch your thighs with your hands, they would feel cold, even though they're actually warm?

Why the paradox?

Why do your lower legs feel cold, yet they feel hot by the touch of your hand? It's because they are conducting heat. This is the reason why they feel cold, yet are hot when touched, at the same time. And observe your thighs. They are opposite. Your thighs feel cold when touched by hand, yet they feel warm inside.

Observe the fat-distribution on the legs. Examine the lower legs. And examine the upper legs.

It's because the thighs are conserving heat. There is more fat around your thighs, thus this functions as insulation keeping your thighs from getting cold.

For men, the lower-legs are almost devoid of fat. Especially in the front of your lower-legs. There is barely any fat covering there. No insulation. This is why your lower-legs get cold easily.

So your lower-legs should require more insulation. A garment which is perfect for this is leg warmers. They should only cover your lower legs, and not your thighs.

Why leg warmers, but not long johns? First of all, long johns overheat your testicles. Long johns also overheat your thighs, because they are typically warmer than your lower-legs, due to the insulating fat on your thighs.

Alternatively, a pair of thick socks or calf boots would work.

Cold legs restrict circulation, producing lactic acid as a byproduct. In addition to the restricted circulation, cold legs have muscles which shiver. This overstresses your leg muscles which leads you to produce even more lactic acid. I believe this is partly why you feel like shit in the morning in bed. You just can't wake up. You tend to believe that this is worse during winter time.

Sleep with your leg warmers on, too. I have observed that slept better when I kept my lower-legs warm, with extra blankets there, without waking up in the morning feeling like I can't get up.

Friday, January 20, 2012

What to Eat on Vacations

Do you fart a lot when you are vacationing? Well, it's probably the foods that make you fart on vacations.

For instance, eating ice cream will make you fart. A lot. Even while in the car. Your car will smell like shit. That shit will annoy your airline passengers, too. Stop that shit.

I'm not suggesting to avoid ice cream. No. Just don't eat ice cream which has carrageenan, so you won't experience those effects. Other side effects I have experienced with low-quality ice cream, are fatigue and acne. The wrong milkshake would cause the same effect.

When I was on vacation, I can't find any orange juice. Well, I actually can find orange juice, but all of them say "from concentrate." I don't like concentrate juice. So it's just that I could not find orange juice which was not from concentrate. Anyway, I went to gas stations. I went to the local stores there. I found nothing. The only thing I found was the "juice from concentrate." Sigh. Guess I was concentrating too much.

But plenty of milk exists on the counters. Bananas. Oh, bananas are widely available. And they're cheap, palatable, and easy-to-store. In fact, bananas are the third most popular fruit in North America. Probably it's because bananas are a "convenience food": What we mean is that they're cheap, widely available, palatable, and energy-dense. They are easy-to-prepare, too. You just peel the banana with your hands. However, bananas may have toxins. The serotonin in bananas, which is harmful, may be an abundance. The starch of bananas, if unripe, could feed gut flora. And the seeds of the banana may cause problems. Bananas are a common food in hotel breakfasts. Probably because bananas are a cheap food for their customers.

In addition to bananas, coffee is also a common food in hotels. Coffee and bananas would make the perfect hotel breakfast. Pour a lot of sugar into the coffee. Drink the coffee with bananas, and add a bit of salt into the coffee to balance the potassium in the bananas.

In fact, the first time I drank coffee was from a hotel. That took away my coffee-virginity. Interestingly, it happened only a year ago. I love hotel breakfasts.

Bananas & Coffee: The perfect hotel breakfast.

Monday, December 26, 2011

My Fetishes II

Below is a list of my sexual fetishes. Items which are labeled "New!" are my recently acquired fetishes.

  • diapers New!
  • wheelchairs
  • anesthesia
  • sneakers
  • women's Keds
  • women's Converse
  • strappy sandals
  • gladiator sandals
  • feet
  • toes New!
  • anklets
  • bangles
  • contact lenses
  • clip-on microphones
  • pantyhose/tights
  • short shorts
  • training wheels
  • trampling
  • foot worship
  • female dominance
  • long striped socks
  • leggings New!
  • skinny jeans New!
  • pedal pumping (on car, piano, and sewing machine)
  • foot play
  • booty shorts New!
  • plastic flip-flops
  • Birkenstocks
  • intravenous injection
  • colorful socks New!
  • putting on pantyhose, tights, and skinny jeans

Wednesday, November 30, 2011

Vitamin and Mineral Supplements: The Preferred Forms

The preferred form of Vitamin B-1 is Thiamine Diphosphate or Thiamine Pyrophosphate.

The preferred form of Vitamin B-2 is Riboflavin 5'-Phosphate.

The preferred form of Vitamin B-3 is Niacinamide.

The Preferred Form of Vitamin B-6 is Pyrioxidal 5'-Phosphate.

The preferred Form of Folate is Methylfolate. (Or at least Calcium Folinate.)

The preferred Form of Vitamin B-12 is Methylcobalamin.

A significant percentage of the population cannot convert the inactive forms of the B-vitamins, to the active forms of the B-vitamins. Therefore, I think it's plausible to get the preferred forms of the B-vitamins.

I have seen no commercial multi-vitamin product, or otherwise any B-complex, which has the preferred forms of all of the B-vitamins

Those other the nutrients related to the B-Vitamins:

Biotin Inositol Choline Para-Aminobenzoic Acid N-Acetyl-Cysteine R-Lipoic Acid Carnitine Carnosine Taurine Beta-Alanine Betaine

Choline, biotin, inositol, carnotine, carnosine, taurine, beta-alanine, and beta-alanine could protect against fatty liver disease. This has been shown in rats.

Carnosine could quench hydroxyl radicals. Free iron ions, or pooly-liganded iron, could react with oxidants, to form hydroxyl radicals. For instance, iron could react with hydrogen peroxide, to form hydroxyl radicals. The hydroxyl radicals are more damaging; as it could cause lipid peroxidation and deplete vitamin E. Carnosine could neutralize hydroxyl radicals, therefore it's an antioxidant, sparing vitamin E, and protecting against the effects of excess iron.

Zinc is a relatively non-toxic metal, and could be supplemented in cases of zinc deficiency or poor soil quality. Zinc oxide and zinc carbonate are poorly-absorbed, as they are not soluble in water. Therefore, they are not the preferred forms of zinc.[9] Preferred forms of zinc include zinc citrate, zinc picolinate, and zinc gluconate. Zinc sulphate is preferred likewise, but it could cause intestinal irritation.[9]

Zinc also reduces nitric oxide synthase, supports immune function, and inhibits aromatase, an enzyme which converts testosterone to estrogen.

Selenium supplementation: Do not get anything other than "selenomethionine" or "selenium from yeast." Any other form of selenium is more damaging. Damaging forms of selenium include "sodium selenate", "sodium selenite", "chelated selenium" and "selenium glycinate." Those forms of selenium are unmethylated, and they are toxic since unbound selenium ions are highly reactive and cause free radical damage.

[1] The Essential Toxin: Impact of Zinc on Human Health Laura M. Plum, Lothar Rink and Hajo Haase * http://www.mdpi.com/1660-4601/7/4/1342/pdf

[2] Zinc supplementation in oral rehydration solutions: experimental assessment and mechanisms of action. Altaf W, Perveen S, Rehman KU, Teichberg S, Vancurova I, Harper RG, Wapnir RA. http://www.ncbi.nlm.nih.gov/pubmed/11838884

Zinc deficiency is associated with chronic diarrhea. This condition is generally linked to an overproduction of nitric oxide (NO), which induces secretion and cellular damage as a free radical.

[3] Zinc-Altered Immune Function and Cytokine Production1 Lothar Rink2 and Holger Kirchner http://jn.nutrition.org/content/130/5/1407S.long

[4] M.A. Beck, P.C. Kolbeck, Q. Shi, L.H. Rohr, V.C. Morris, and O.A. Levander, “Increased Virulence of a Human Enterovirus (Coxsackievirus B3) in Selenium-Deficient Mice”, J. Infectious Diseases 170, 351-357, 1994. [2] M.A. Beck, P.C. Kolbeck, L.H. Rohr, Q. Shi, V.C. Morris, and O.A. Levander, “Vitamine E Deficiency Intensifies the Myocardial Injury of Coxsackievirus B3 Infection of Mice”, J. Nutr.

This effect is reversed with selenium deficiency. Older mice that are also selenium deficient are as susceptible to the virus as young mice.

These tests employ lard, special fish oil with vitamin E removed, selenium and vitamin E. The vitamin E prevents the deleterious formation of aliphatic hyperperoxides from the high concentrations of unsaturated fatty acids in the fish oil. Fish oil administered without vitamin E depletes the body's store of vitamin E and potentiates the heart damage observed with the virus infection. (Normal fish oil contains a small but sufficient amount of vitamin E to prevent these problems.)

http://www.philsoc.org/1995Spring/2041minutes.html

[5] J Nucleic Acids. 2010 Sep 22;2010. pii: 725071. Prevention of mutation, cancer, and other age-associated diseases by optimizing micronutrient intake. Ames BN. http://www.ncbi.nlm.nih.gov/pubmed/20936173

[6] FASEB J. 2011 Jun;25(6):1793-814. Epub 2011 Mar 14. Adaptive dysfunction of selenoproteins from the perspective of the triage theory: why modest selenium deficiency may increase risk of diseases of aging. McCann JC, Ames BN.

[7] Arther & Beckett. (1999) Thyroid function http://bmb.oxfordjournals.org/content/55/3/658.abstract?ijkey=142d514bc098871f0edbf58f0989a55060f2627a&keytype2=tf_ipsecsha

[8] Arther & Beckett. (2004) Selenium and endocrine systems http://joe.endocrinology-journals.org/content/184/3/455.abstract?ijkey=62929d24abdd3d8eb6509950b387320efd616459&keytype2=tf_ipsecsha+html

[9] Zinc and micronutrient supplements for children LH Allen - The American journal of clinical nutrition, 1998 - Am Soc Nutrition

How to Lose Fat without Dieting

Sodium, magnesium, and calcium are a definite "yes." All of those minerals have indisputable evidence that they help to reduce stress.

Sodium reduces the RAAS system and vasopresson. All those systems have been shown to cause inflammation, oxidative stress, and artheroscoleosis.

Magnesium and calcium shuts down PTH, which also have those beneficial effects. David McCarron and others have showed that calcium releives hypertension.

Short-chain and medium-chain saturated fatty acids have indisputable evidence that they are anti-microbial and are metabolically enhancing. However, they are not necessarily for a healthy diet, if you are already PUFA deficient or have good microflora.

Corticosteroids have indisputable evidence that they slow down oxidative metabolism, causes excitation, and calcification of tissues. Adrenaline and noradrenaline have indisputable evidence that they, too, causes this. Estrogen increase corticosteroids, adrenaline, and noradrenaline, via the stimulation of the pituitary and hypothalamus to increase ACTH, or directly stimulate the conversion of cholesterol into corticosteroids in the adrenal glands. Free fatty acids could contribute to corticosteroid stimulation via a positive feedback loop. Estrogen also inhibits the detoxification of adrenaline, noradrenaline, and serotonin via its inhibition of MAO.

Estrogen has been claimed to be protective of Alzheimer's, stroke, hypertension, osteoporosis, and heart disease. However, those protective effects come with a cost of increased nitric oxide, corticosteroids, and catecholamines. A lot of the beneficial effects of estrogen supplementation (e.g. soy) are falsely attributed to the estrogen itself.

High estrogen levels are caused by zinc deficiency, inflammatory eicosanoids, interleukin, and fat mass. Decreased estrogen clearance could be cased by liver congestion, energy deficiency, B-vitamin deficiency, or protein deficiency. Biskind and Biskind showed how B-vitamin and protein deficiency could interfere with the detoxification of estrogen.

Carbon dioxide has been shown to be protective. It's anti-inflammatory and an antioxidant. Speeding up oxidative metabolism raises carbon dioxide retention. Also, maintaining a normal pH also retains carbon dioxide.

Ammonia is toxic. Ammonia is produced when there is not enough minerals such as calcium, magnesium, sodium, and potassium. A diet suffecient with those minerals clears ammonia. Glucose also helps to reduce ammonia.

Amylase is an enzyme which breaks down starch. Different people have different amylase enzymes. The Japanese have more amylase enzymes encoded in their genes than hunter-gatherers. This shows that amylase is selectively advantegous. Amylase is selectively advantagous because it breaks down the starch into mono- and disaccharides, which are less prone to cause endotoxin and intestinal inflammation. So it suggests that it may be more healthful to eat simple sugars rather than starch. However, it's physiological significance is questioned, as improved digestion could break down the starch entirely into its constituent monosaccharides.

Glycine relaxes the neurons, prevents neuron excitation, and the activation of the HPA axis. In contrast, glutamate and aspartate has the opposite of glycine's effects. Glycine also helps to store glycogen. This effect is shared with adenosine, too.

Tryptophan has shown to cause decreased lifespan, and serotonin release.

Caffeine has been therapeutic in inflammation and caffeine can function as an anti-oxidant due to its similarity to uric acid and its effect in inhibiting xanthine oxidase, which generates free radicals.

A1 milk and gluten are questionable, because even if you have perfect digestion, they could still irritate the intestines and cause inflammation and a leaky gut; unless your salivary and gastric enzymes break down A1 beta casein or gluten, entirely, into its constituent amino acids, before it enters the duodenum.

Fructose is good, at it helps to normalize blood sugar by repleshing liver glycogen, or to increase thyroid conversion. However, fructose has been claimed to cause glycation about seven times fater than glucose. However, it's physiological significance is questioned.

Based on the indisputable evidence, a safe diet is a diet based on salt, magnesium, calcium, coconut oil, ghee, vinegar, and cooked starch. Sufficient protein and B-vitamins should help with liver function. Monosodium glutamate and aspartame should be avoided. Glycine and proline-rich foods (such as collagen) should be supplemented. Baking soda, magnesium citrate, and calcium carbonate as supplements, digestive enzymes, systemic enzymes, and mixed tocopherols as supplements.

White rice, potatoes, white-fleshed sweet potatoes, taro, yams, and others. Oysters for zinc.

Limit tryptophan, methionine, and cysteine.

Sufficient iodine and selenium. Milk is a good source of iodine, containing 60 mcg per cup.

Blood donation. Iron has been shown to react with endogenous oxidants to produce even more dangerous free radicals. Serum ferritin should be between 30-40. Anthony Colpo commenter claimed that 30 is not enough - they had exhaustion. And Bruce Ames hypothesized that iron deficiency causes aging.

Tamoxifen is estrogenic.

Aspirin, coffee, and niacinamide as supplements. However, synthetic vitamins should be taken cautiously.

Supplementation with the digestive enzyme, DPP IV, by helping with the breakdown of allergic peptides, has been therapeutic in Celiac disease, and milk intolerance. In addition, DPP IV enzymes have been used to treat autism and ADHD, as they have been known to have gluten and casein intolerance, elevated serotonin, and lowered DPP IV production. However, possible allergens in the production of the DPP IV enzyme, or to an allergy to the bacteria, are not unheard of.

Food colorings are known to inhibit digestive enzymes, thus exacerbating the inflammatory cycle. In cases such as ADHD, food colorings has been know to exacerbate those symptoms. For instance, "caramel color" in coke might inhibit digestive enzymes, causing systemic inflammation. Sodium benzoate, an ingredient in coke, is a known digestive enzyme inhibitor, and it is known to deplete glycine.

All those are just based on that evidence alone.

REFERENCES

Plasma levels of alpha-tocopherol, gamma-tocopherol, beta-cryptoxanthin, and lutein were also higher in the winter and lower in the summer. Curr Med Chem. 2004 May;11(9):1113-33. Non-antioxidant activities of vitamin E. Zingg JM, Azzi A.

Is vitamin E an antioxidant, a regulator of signal transduction and gene expression, or a ‘junk’ food? Comments on the two accompanying papers: “Molecular mechanism of α-tocopherol action” by A. Azzi and “Vitamin E, antioxidant and nothing more” by M. Traber and J. Atkinson

Regina Brigelius-Flohéa, Kelvin J.A. Davies

Tocopherols and tocotrienols in membranes: A critical review Jeffrey Atkinsona, , , Raquel F. Epandb, Richard M. Epandb

RELATION BETWEEN SERUM AND URINARY CALCIUM WITH PARTICULAR REFERENCE TO PARATHYROID ACTIVITY M. Peacock, W.G. Robertson, B.E.C. Nordin

VitRELATION BETWEEN SERUM AND URINARY CALCIUM WITH PARTICULAR REFERENCE TO PARATHYROID ACTIVITY

M. Peacock, W.G. Robertson, B.E.C. Nordinamin D deficiency and renal calcium transport in the rat. M Yamamoto, Y Kawanobe http://www.ncbi.nlm.nih.gov/pmc/articles/PMC370503/pdf/jcinvest00710-0203.pdf

Calcium-regulated renal calcium handling in healthy men: relationship to sodium handling http://jcem.endojournals.org/content/83/7/2366.full

Milk alkali syndrome and the dynamics of calcium homeostasis [HTML] from asnjournals.org AJ Felsenfeld http://cjasn.asnjournals.org/content/1/4/641.full

Calcium clamp technique: suppression of serum intact PTH by induced hypercalcaemia in normal man and primary hyperparathyroidism

Bioconversion of dietary provitamin A carotenoids to vitamin A in humans1,2,3,4,5 Guangwen Tang http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854912/

EFFECT OF ZINC AND FAT INTAKE ON ABSORPTION AND CONVERSION OF INGESTED ß-CAROTENE TO VITAMIN A IN LACTATING INDONESIAN WOMEN

Effects of short-term administration of growth hormone in healthy young men, women, and women taking oral contraceptives B. Edén Engström, P. Burman, A. G. Johansson, L. Wide, F. A. Karlsson http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2000.00672.x/full

EFFECTS OF OESTROGEN AND PROGESTERONE ON AGE-RELATED CHANGES IN ARTERIES OF POSTMENOPAUSAL WOMEN Yu-Lu Liang1, Helena Teede1, Louise M. Shiel1, Adrian Thomas2, Robyn Craven3, Nirupa Sachithanandan1, John J. McNeil2, James D. Cameron4, Anthony Dart5, Barry P. McGrath1,* Article first published online: 28 JUN 2007 http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1681.1997.tb01225.x/abstract

Effects of estrogen on gender-related autonomic differences in humans C. C. Liu,1,* Terry B. J. Kuo,2,4,* and Cheryl C. H. Yang3 http://ajpheart.physiology.org/content/285/5/H2188.full

Effects of estrogens and progestogens on the renin-aldosterone system and blood pressure Wolfgang K.H. Oelkers http://www.sciencedirect.com/science/article/pii/0039128X96000074

"High dose estrogens, especially ethinylestradiol (EE) and mestranol, stimulate the synthesis of hepatic proteins including coagulation factors, sex hormone binding globulin, and angiotensinogen (Aogen). In the steady state, high plasma levels of Aogen produce only a very small increase of angiotensin II (AII) and plasma renin activity, because AII inhibits the secretion of renin and lowers plasma renin concentration. However, the increase in AII is sufficient for a slight reduction in renal blood flow and a slight increase in exchangeable sodium and blood pressure; in susceptible women, blood pressure may rise considerably.

"Synthetic progestogens are commonly devoid of the mineralocorticoid receptor antagonistic effect of progesterone, and some are weak estrogen receptor agonists.

The metabolic clearance rate of progesterone in males and ovariectomized females. B Little, J F Tait, S A Tait, and F Erlenmeyer http://www.ncbi.nlm.nih.gov/pmc/articles/PMC292769/

Effects of sex steroid hormones on regional fat depots as assessed by magnetic resonance imaging in transsexuals J. M. H. Elbers1, H. Asscheman1, J. C. Seidell2, and L. J. G. Gooren1 http://ajpendo.physiology.org/content/276/2/E317.short

Progesterone Antagonists Increase Androgen Receptor Expression in the Rhesus Macaque and Human Endometrium http://jcem.endojournals.org/content/86/6/2668.full

Exogenous Progesterone Attenuates the Subjective Effects of Smoked Cocaine in Women, but not in Men Suzette M Evans1 and Richard W Foltin1 http://www.nature.com/npp/journal/v31/n3/abs/1300887a.html

Adrenocorticotropin and Cortisol-Induced Changes in Urinary Sodium and Potassium Excretion in Man: Effects of Spironolactone and RU486 http://jcem.endojournals.org/content/67/4/824.short

Estrogenic encounters: How interactions between aromatase and the environment modulate aggression Brian C. Trainor,a* Helen H. Kyomen,b and Catherine A. Marlerc

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080681/

Effects of progestins on sexual behaviour in castrated lizards (Cnemidophorus inornatus) J. Lindzey and D. Crews http://joe.endocrinology-journals.org/content/119/2/265.short

Progesterone receptors mediate male aggression toward infants Johanna S. Schneider*, Marielle K. Stone*, Katherine E. Wynne-Edwards†, Teresa H. Horton*, John Lydon‡, Bert O'Malley‡, and Jon E. Levine*§ http://www.pnas.org/content/100/5/2951.full

"High T levels, however, do not necessarily decrease paternal behavior in many species (1, 2) and even promote paternal behavior in the California mouse, Peromyscus californicus (3) via aromatization to estrogen (4). Furthermore, T levels do not correlate with paternal behavior in common laboratory mice (5). In humans, some fathers experience a decrease in T levels immediately after birth of a child (6, 7); however, its association with paternal behaviors is not known.

"Although male Cynomolgus monkeys exhibit increased male-male aggression after medroxyprogesterone acetate (MPA) treatments (35), the specific effects of this progestin on infant-directed aggression in male primates have not been examined.

PROGESTERONE AND HETEROTYPICAL SEXUAL BEHAVIOUR IN MALE RATS J. M. DAVIDSON and S. LEVINE http://joe.endocrinology-journals.org/content/44/1/129.short "Male rats castrated during the first few days of life, but not later, show behavioural responses closely resembling those of normal females after treatment with ovarian steroids in adulthood. This suggests that testicular secretion in the neonatal period is responsible for the determination of future behavioural patterns (Grady, Phoenix & Young, 1965;

Sexual orientation in women: An investigation of hormonal and personality variables☆ C.P. Dancey http://www.sciencedirect.com/science/article/pii/030105119090142J

Testicular function in transsexual men Although the sperm counts of 5 of 8 adult male-to-female transsexuals were low, other aspects of testicular function were normal. Plasma production rates of testosterone averaged 6.4 mg/24 hours, a value similar to the 5.7 mg/24 hours produced by heterosexual adult men. Production rates of 17-estradiol and estrone, 55µg/24 hours and 52 µg/24 hours, were also normal. Observed abnormalities of pituitary function and pituitary response to LHRH cannot be explained by abnormal testicular steroidogenesis.

"A technique of incubation of testicular tissue in vitro with radiolabeled precursors was applied in the investigation of the steroid biosynthesis by testes of four young men after long-term, high-dose estrogen treatment. A positive correlation between plasma and testicular steroid levels, and in vitro capacity of the testes to metabolize progesterone was demonstrated.

"Estrogen administration produced a very significant inhibition of plasma and testicular levels of testosterone. The in vitro synthesis of testosterone from progesterone was very severely impaired; especially 17α-hydroxylation of progesterone. 20α-hydroxysteroid-dehydrogenase activity was found to be increased after estrogen treatment, both in vivo and in vitro.

Fed Proc. 1959 Dec;18:1057-65. Effects of progesterone and synthetic progestins on the reproductive physiology of normal men. HELLER CG, MOORE DJ, PAULSEN CA, NELSON WO, LAIDLAW WM.

Optimal Waist-to-Hip Ratios in Women Activate Neural Reward Centers in Men Steven M. Platek1*, Devendra Singh2 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0009042

Seasonal Variation of Testosterone and Waist to Hip Ratio in Men: The Tromsø Study Johan Svartberg, Rolf Jorde, Johan Sundsfjord, Kaare H. Bønaa and Elizabeth Barrett-Connor http://jcem.endojournals.org/content/88/7/3099.short

"Lowest testosterone levels occurred in months with the highest temperatures and longest hours of daylight. Waist to hip ratio paralleled the change in daylight and temperature, with the highest values during the summer and was thus inversely related to the seasonal testosterone variation.

Progesterone, prolactin, and gynaecomastia in men with liver disease. M J Farthing, J R Green, C R Edwards, A M Dawson http://gut.bmj.com/content/23/4/276.abstract

"Plasma progesterone was raised in 36 of 50 (72%) men with liver disease compared with 20 healthy male control subjects. Plasma progesterone was significantly higher in men with non-alcoholic cirrhosis with gynaecomastia than those without, but no similar relationship was found in men with alcoholic fatty change and alcoholic cirrhosis. Hyperprolactinaemia was found in 14% of men with liver disease but levels were unrelated to the presence of gynaecomastia. Increased circulating levels of progesterone and prolactin alone do not explain the development of gynaecomastia in patients with liver disease, but progesterone may be an additional factor acting in association with the known disturbances of other sex steroids.

Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels Jacob C. Seidell , a, b, c, d, 1, Per Björntorpa, b, c, d, Lars Sjöströma, b, c, d, Henry Kvista, b, c, d, Rune Sannerstedta, b, c, d http://www.sciencedirect.com/science/article/pii/002604959090297P

Progesterone: the forgotten hormone in men? M Oettel1 and AK Mukhopadhyay2 1Jena http://informahealthcare.com/doi/abs/10.1080/13685530400004199 "A progestin may stimulate weight gain and appetite in men as well as in women.

Effect of sex on the strain differences in hepatic metabolism of starved and nonstarved rats http://jn.nutrition.org/content/109/2/272.full.pdf

Biotin supplementation reduces plasma triacylglycerol andáVLDL inátype 2ádiabetic patients andáinánondiabetic subjects with hypertriglyceridemia http://www.sciencedirect.com/science/article/pii/S0753332206000539

Effects on biotin, fat type and sodium nitrite on organ size, plasma constituents and liver fatty acid composition in rats* http://www.sciencedirect.com/science/article/pii/S0271531785801743

The potential role of biotin insufficiency on essential fatty acid metabolism and cardiovascular disease risk http://www.direct-ms.org/pdf/EvolutionPaleolithic/Biotin%20Paper.pdf

Dietary biotin effects on desaturation and elongation of 14C-linoleic acid in the chicken http://www.sciencedirect.com/science/article/pii/S027153170580274X

5 - Hormones and the Development and Expression of Aggressive Behavior B.C. Trainor, C.L. Sisk, R.J. Nelson http://www.sciencedirect.com/science/article/pii/B978008088783800005X

"Throughout the chapter, a comparison is made between the regulation of rodent animal models of aggression and human aggression with the goal of emphasizing where further research is needed to understand nonadaptive or pathological aggression.

Activation of aggressive behavior by progesterone and testosterone in male tree lizards, Urosaurus ornatus

S.L Weiss , , M.C Moore http://www.sciencedirect.com/science/article/pii/S0016648004000024

Changes in brain testosterone and allopregnanolone biosynthesis elicit aggressive behavior Graziano Pinna *, Erminio Costa, and Alessandro Guidotti http://www.pnas.org/content/102/6/2135.long

Effects of estrogens and progestogens on the renin-aldosterone system and blood pressure WKH Oelkers - Steroids, 1996 - Elsevier Endogenous 17β-estradiol (E2) and low parenteral doses of exogenous E2 are vasodilators. High dose estrogens, especially ethinylestradiol (EE) and mestranol, stimulate the synthesis of hepatic proteins including coagulation factors, sex hormone binding globulin, and ... Cited by 172 - Related articles - BL Direct - All 6 versions http://www.sciencedirect.com/science/article/pii/0039128x96000074

Comment on progesterone effects in breast tissue http://www.springerlink.com/content/x125660612190317/

Progesterone modulation of androgen-dependent sexual behavior in male rats

Diane M. Witt , ∗, Larry J. Young†, David Crews†

"Mounting was observed in 75% of the T-alone males. More than half (64%) of the P-atone males and 100% P + T males exhibited mounting. In most cases, mounting was followed by intromission responses. Subsequently, intact and gonadectomized males received daily injections of the P antagonist RU486 along with hormone treatment. After receiving RU486, only 63% of the intact males and 71 % of the T-alone males mounted successfully. The facilitatory effects of P on copulatory behavior were completely abolished by RU486 treatment. The present studies provide the first evidence in mammals suggesting that P-dependent mechanisms influence neurochemical pathways involved in copulation.

Modulation by estradiol of serotonin receptors in brain A Biegon and BS McEwen http://www.jneurosci.org/content/2/2/199.full.pdf+html

Estrogens were found to exert a biphasic effect on the density of serotonin receptors in the female rat brain: an acute reduction in serotonin receptor density throughout the brain is followed 48 to 72 hr later by a selective increase in those brain regions known to contain estrogen receptors--hypothalamus, preoptic area, and amygdala. The acute reduction in serotonin receptor density can be mimicked by estradiol in vitro. We conclude that estradiol may have a fast, direct effect on brain membranes to modify serotonin receptor availability, while exerting a slow effect on the same receptors through an interaction with intracellular estrogen receptors in those brain regions that contain them. The observation that female sex hormones are involved in the regulation of serotonin receptors may have important implications in the understanding of female sexual behavior in the female rat and in the understanding of hormone-linked emotional disturbances in women

Estradiol-17 [beta] increase serotonin transporter (SERT) mRNA levels and the density of SERT-binding sites in female rat brain JK McQueen, H Wilson… - Molecular brain research, 1997 - Elsevier

Effects of estradiol and progesterone administration on human serotonin 2A receptor binding: a PET study EL Moses, WC Drevets, G Smith, CA Mathis http://directory.umm.ac.id/Data%20Elmu/jurnal/B/Biological%20Psichatry/Vol48.Issue8.2000/6836.pdf

Estradiol-17β increase serotonin transporter (SERT) mRNA levels and the density of SERT-binding sites in female rat brain Judith K. McQueen , Helen Wilson, George Fink

Effects of chronic 17β-estradiol treatment on the serotonin 5-HT1A receptor mRNA and binding levels in the rat brain Marie K. Österlund, Christer Halldin, Yasmin L. Hurd http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1098-2396(200001)35:1%3C39::AID-SYN5%3E3.0.CO;2-T/abstract

Thus, the previous findings together with the present results indicate that estradiol-induced alterations in 5-HT1A receptor mRNA expression appears within hours, but diminishes with chronic treatment when significant changes on the receptor-protein level are apparent.

Estrogen actions in the central nervous system [PDF] from uwks.ac.id Free from Publisher BS McEwen http://www.fk.uwks.ac.id/elib/Arsip/Departemen/Biokimia/Estrogen%20Actions%20in%20the%20Central%20Nervous%20System.pdf

M.A. Beck, P.C. Kolbeck, Q. Shi, L.H. Rohr, V.C. Morris, and O.A. Levander, “Increased Virulence of a Human Enterovirus (Coxsackievirus B3) in Selenium-Deficient Mice”, J. Infectious Diseases 170, 351-357, 1994. M.A. Beck, P.C. Kolbeck, L.H. Rohr, Q. Shi, V.C. Morris, and O.A. Levander, “Vitamine E Deficiency Intensifies the Myocardial Injury of Coxsackievirus B3 Infection of Mice”, J. Nutr.

This effect is reversed with selenium deficiency. Older mice that are also selenium deficient are as susceptible to the virus as young mice.

These tests employ lard, special fish oil with vitamin E removed, selenium and vitamin E. The vitamin E prevents the deleterious formation of aliphatic hyperperoxides from the high concentrations of unsaturated fatty acids in the fish oil. Fish oil administered without vitamin E depletes the body's store of vitamin E and potentiates the heart damage observed with the virus infection. (Normal fish oil contains a small but sufficient amount of vitamin E to prevent these problems.)

Metabolism of Linoleic Acid by Human Gut Bacteria: Different Routes for Biosynthesis of Conjugated Linoleic Acid Estelle Devillard, Freda M. McIntosh, Sylvia H. Duncan, and R. John Wallace* http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1899373/

Differences between human subjects in the composition of the faecal bacterial community and faecal metabolism of linoleic acid Estelle Devillard1,†, Freda M. McIntosh1, Delphine Paillard1, Nadine A. Thomas1, Kevin J. Shingfield2 and R. John Wallace1 http://mic.sgmjournals.org/content/155/2/513.full

Prevent Osteoporosis with Egg Shell Calcium, Vitamins D and K2, and Other Nutrients http://www.smart-publications.com/articles/prevent-osteoporosis-with-egg-shell-calcium-vitamins-d-and-k2-and-othe/page-2

serotonin + the thromboxane analog U-46619, in estrogen-deprived VMC were suppressed by >72 h in 17-estradiol. http://ajpheart.physiology.org/content/290/1/H295.short

Calcium paradox of aldosteronism and the role of the parathyroid glands Alex Vidal,1 Yao Sun,1 Syamal K. Bhattacharya,3 Robert A. Ahokas,4 Ivan C. Gerling,2 and Karl T. Weber1 http://ajpheart.physiology.org/content/290/1/H286.full

Is hypovitaminosis D one of the environmental risk factors for multiple sclerosis? http://brain.oxfordjournals.org/content/133/7/1869.short

Nat Cell Biol. 2008 May;10(5):611-8. Epub 2008 Apr 6. p53 regulates glucose metabolism through an IKK-NF-kappaB pathway and inhibits cell transformation. Kawauchi K, Araki K, Tobiume K, Tanaka N. http://www.ncbi.nlm.nih.gov/pubmed/18391940

Am J Physiol Heart Circ Physiol. 2003 Mar;284(3):H1028-34. Epub 2002 Nov 21. Endotoxemia stimulates skeletal muscle Na+-K+-ATPase and raises blood lactate under aerobic conditions in humans. Bundgaard H, Kjeldsen K, Suarez Krabbe K, van Hall G, Simonsen L, Qvist J, Hansen CM, Moller K, Fonsmark L, Lav Madsen P, Klarlund Pedersen B. http://www.ncbi.nlm.nih.gov/pubmed/12446281

Biochem Pharmacol. 1995 Jan 6;49(1):65-8. Endotoxin inhibits glucuronidation in the liver. An effect mediated by intercellular communication. Bánhegyi G, Mucha I, Garzó T, Antoni F, Mandl J. http://www.ncbi.nlm.nih.gov/pubmed/7840784

Effects of catecholamines on lactic acid output during progressive working contractions. by W N Stainsby, C Sumners, P D Eitzman http://www.mendeley.com/research/effects-catecholamines-lactic-acid-output-during-progressive-working-contractions/

Agressologie. 1973;14(1):25-30. [Aspirin, catecholamines and blood lactic acid]. [Article in French] Laborit G, Baron C, Laborit H.

Nutr Metab. 1976;20(1):41-61. Biotin status and lipid metabolism in adult obese hypercholesterolemic inbred rats. Marshall MW, Haubrich M, Washington VA, Chang MW, Young CW, Wheeler MA. http://www.ncbi.nlm.nih.gov/pubmed/958648

Aldosterone regulation of T-type calcium channels☆

Michel F Rossiera, b, , , Olivier Lesouhaitiera, Emeline Perriera, Liliane Bockhorna, Alberto Chiappeb, Nathalie Lalevéea http://www.sciencedirect.com/science/article/pii/S0960076003002012

Effects of estradiol and progesterone on the increased synthesis of collagen in atherosclerotic rabbit aortas☆ G.M. Fischer, M.L. Swain∗ http://www.sciencedirect.com/science/article/pii/0021915085901777

Effects of Progesterone and Four Synthetic Progestagens on Sodium Balance and the Renin-Aldosterone System in Man*

"50 mg of progesterone im caused, as expected, natriuresis, an increase in plasma renin activity (PRA), plasma angiotensin II concentration (PAC) and aldosterone excretion (AER), while plasma renin substrate concentration (PRS) remained unchanged.

Horm Metab Res. 2005 Jul;37(7):455-9. Aldosterone inhibits uncoupling protein-1, induces insulin resistance, and stimulates proinflammatory adipokines in adipocytes. Kraus D, Jäger J, Meier B, Fasshauer M, Klein J. http://www.ncbi.nlm.nih.gov/pubmed/16034720

Effects of estrogens and progestogens on the renin-aldosterone system and blood pressure Wolfgang K.H. Oelkers http://www.sciencedirect.com/science/article/pii/0039128X96000074

"Endogenous 17β-estradiol (E2) and low parenteral doses of exogenous E2 are vasodilators. High dose estrogens, especially ethinylestradiol (EE) and mestranol, stimulate the synthesis of hepatic proteins including coagulation factors, sex hormone binding globulin, and angiotensinogen (Aogen).

"Endogenous progesterone is a mineralocorticoid receptor antagonist. Endogenous or exogenous progesterone leads to sodium loss and a compensatory increase in renin secretion, plasma renin activity, AII, and plasma aldosterone, e.g. in the second half of the menstrual cycle. Synthetic progestogens are commonly devoid of the mineralocorticoid receptor antagonistic effect of progesterone, and some are weak estrogen receptor agonists.

Pediatr Nephrol. 1992 May;6(3):313. Normal ranges for urinary excretion of calcium and magnesium in Portuguese children. Sa G, Proença H, Rosa FC. http://www.springerlink.com/content/tp60q38002436510/

Absorption of Calcium as the Carbonate and Citrate Salts, with Some Observations on Method http://www.springerlink.com/content/dx8kyt8u2t0xm37l/ Absorbability of calcium from the carbonate and citrate salts was compared at 300 mg and 1000 mg calcium loads, ingested as part of a light breakfast meal.

Calcium Absorption Varies within the Reference Range for Serum 25-Hydroxyvitamin D Robert P. Heaney, MD, FACN, M. Susan Dowell, PhD, Cecilia A. Hale, PhD and Adrianne Bendich, PhD, FACN

"AUC9 (± SEM), was 3.63 mg hr/dL ± 0.234 in participants pretreated with 25OHD and 2.20 ± 0.240 in those not pretreated (P < 0.001). In brief, absorption was 65% higher at serum 25OHD levels averaging 86.5 nmol/L than at levels averaging 50 nmol/L (both values within the nominal reference range for this analyte).

Urinary calcium excretion in Swedish children E Esbjorner1,*, IL Jones2

Dietary salt, urinary calcium, and bone loss Linda K. Massey1,*, Susan J. Whiting2 http://onlinelibrary.wiley.com/doi/10.1002/jbmr.5650110603/abstract

Changes in Serum and Urinary Calcium during Treatment with Hydrochlorothiazide: Studies on Mechanisms Arnold S. Brickman, Shaul G. Massry, and Jack W. Coburn

Both the reduction in urinary calcium and increase in urinary phosphate after the use of thiazides may be due, in part, to potentiation of the action of the parathyroid hormone on the nephron. The rise in serum calcium could be due to thiazide-induced release of calcium from bone into extracellular fluid, particularly in states where bone resorption may be augmented, i.e., vitamin D therapy or hyperparathyroidism.

Impaired renal calcium absorption in mice lacking calcium channel ß3 subunits José F. Bernardo,* Clara E. Magyar,† W. Bruce Sneddon,† and Peter A. Friedman*† http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955898/

The absence of ß3 subunits resulted in compensatory increases of TrpV5 calcium channels, the plasma membrane Ca-ATPase, NCX1 Na/Ca exchanger protein, and calbindin-D9k but not calbindin-D28k. We conclude that TrpV5 mediates basal renal calcium absorption and that a multimeric calcium channel that includes CaVß3 mediates stimulated calcium transport.

http://www.nejm.org/doi/full/10.1056/NEJM199707103370201 Trial of Calcium to Prevent Preeclampsia Richard J. Levine, M.D., John C. Hauth, M.D., Luis B. Curet, M.D., Baha M. Sibai, M.D., Patrick M. Catalano, M.D., Cynthia D. Morris, Ph.D., Rebecca DerSimonian, Sc.D., Joy R. Esterlitz, M.S., Elizabeth G. Raymond, M.D., Diane E. Bild, M.D., John D. Clemens, M.D., Jeffrey A. Cutler, M.D., Marian G. Ewell, Steven A. Friedman, Robert L. Goldenberg, Sig-Linda Jacobson, Gary M. Joffe, M.D, Mark A. Klebanoff, and Alice S. Petrulis, M.D.

Calcium supplementation did not significantly reduce the incidence or severity of preeclampsia or delay its onset. Preeclampsia occurred in 158 of the 2295 women in the calcium group (6.9 percent) and 168 of the 2294 women in the placebo group (7.3 percent) (relative risk, 0.94; 95 percent confidence interval, 0.76 to 1.16). There were no significant differences between the two groups in the prevalence of pregnancy-associated hypertension without preeclampsia (15.3 percent vs. 17.3 percent) or of all hypertensive disorders (22.2 percent vs. 24.6 percent). The mean systolic and diastolic blood pressures during pregnancy were similar in both groups. Calcium did not reduce the numbers of preterm deliveries, small-for-gestational-age births, or fetal and neonatal deaths; nor did it increase urolithiasis during pregnancy.

EFFECTS OF NATURAL AND ARTIFICIAL MENOPAUSE ON PLASMA AND URINARY CALCIUM AND PHOSPHORUS M.M. Young M.B. Durh., OF THE SCIENTIFIC STAFF, B.E.C. Nordin M.D., Ph.D. Lond., F.R.C.P., DIRECTOR http://www.sciencedirect.com/science/article/pii/S0140673667929613 "It is suggested that loss of œ strogenic activity at the menopause results in increased bone resorption.

Carbonated beverages and urinary calcium excretion1,2,3 Robert P Heaney and Karen Rafferty http://www.ajcn.org/content/74/3/343.long The excess calciuria associated with consumption of carbonated beverages is confined to caffeinated beverages. Acidulant type has no acute effect. Because the caffeine effect is known to be compensated for by reduced calciuria later in the day, we conclude that the net effect of carbonated beverage constituents on calcium economy is negligible.The skeletal effects of carbonated beverage consumption are likely due primarily to milk displacement.

Urinary calcium excretion in healthy school children Laura F. Alconcher, Cecilia Castro, Daniel Quintana, Nancy Abt, Luis Moran, Laura Gonzalez, Mabel Cella and Mabel Torelli http://www.springerlink.com/content/1rx6rc67tmnftjnk/

"The Ca/Cr ratio in the first-morning urine sample correlated poorly with the 24-h calcium excretion, suggesting that the Ca/Cr ratio in first-morning urine samples cannot replace the 24-h measurement.

Urinary calcium and oxalate excretion in children György S. Reusz, Mariann Dobos, Dennis Byrd, Péter Sallay, Miklós Miltényi and Tivadar Tulassay http://www.springerlink.com/content/q287536341qx30q7/

Urinary excretion of calcium and magnesium in children S. Ghazali, T. M. Barratt http://adc.bmj.com/content/49/2/97.abstract After a milk load of 700 ml/1·73 m2 the urinary calcium/creatinine concentration ratio rose in the first two hours, but in no sample exceeded 0·25 mg/mg.

Urinary calcium and calcium balance in young men as affected by level of protein and phosphorus intake M Hegsted, SA Schuette, MB Zemel http://jn.nutrition.org/content/111/3/553.full.pdf

The effect of dietary sodium on urinary calcium and potassium excretion in normotensive men with different calcium intakes JJ Castenmiller, RP Mensink http://www.ajcn.org/content/41/1/52.full.pdf

Effect of estrogens and calcium carbonate on bone loss in postmenopausal women RR RECKER, PD SAVILLE http://www.annals.org/content/87/6/649.short

Urinary excretion of calcium and magnesium in children S. Ghazali and T. M. Barratt http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1648734/

Effect of Estrogens and Calcium Carbonate on Bone Loss in Postmenopausal Women ROBERT R. RECKER, M.D., F.A.C.P.; PAUL D. SAVILLE, M.D., F.A.C.P.; and ROBERT P. HEANEY, M.D., F.A.C.P. [1] these techniques are sufficiently sensitive to detect age-related bone loss; [2] postmenopausal sex-hormone replacement measurably decreases age-related bone loss by suppressing bone turnover, resorption more than accretion; and [3] calcium supplements produce the same effect but at the dose we used were slightly less effective.

Can J Physiol Pharmacol. 1982 Mar;60(3):331-4. Role of acidosis in the protein wasting of fasting in the rat and the rabbit. Hannaford MC, Goldstein MB, Josse RG, Halperin ML. http://www.ncbi.nlm.nih.gov/pubmed/7074421

A Novel Property of Povidon-Iodine: Inhibition of Excessive Protease Levels in Chronic Non-Healing Wounds Sabine A Eming1,3, Sigrun Smola-Hess2,3, Peter Kurschat1, Doris Hirche1, Thomas Krieg1 and Hans Smola1,4 http://www.nature.com/jid/journal/v126/n12/full/5700474a.html

"Iodine is strongly oxidative and easily reacts with the amino, phenol, and –SH groups of amino acids, with unsaturated fatty acids and nucleotides. For enzymes, this results in denaturation and loss of function and we suspect that it is this mechanism we observe in our experiments.

Acta Endocrinol (Copenh). 1981 Dec;98(4):556-63. The effect of varying iodine content on the proteolytic activity of rat thyroid lysosomes. Santisteban P, Lamas L. http://www.ncbi.nlm.nih.gov/pubmed/6272517

"The proteolytic activity of lysosomal fractions from the various experimental groups towards thyroglobulin decreased slightly with increased iodide supply both in chronic and acute experiments. The results suggest that thyroid lysosomal activity may participate in the autoregulation of thyroid secretion by inducing synthesis of new enzymes and modulating thyroglobulin degradation.

J Nutr. 1969 Feb;97(2):246-54. Interrelationship of triglycerides with calcium, magnesium and phosphorus in the rat. Tadayyon B, Lutwak L. http://www.ncbi.nlm.nih.gov/pubmed/5767134 Fat has little to do with the absorption of calcium. Though vitamin D, lactose, protein, antibiotics, and growth hormone. Phytate and phosphate lowers calcium assimilation.

http://www.mgwater.com/bj0198.shtml

Effect of Magnesium Depletion on Responsiveness to Parathyroid Hormone in Parathyroidectomized Rats T. J. Hahn, L. R. Chase, and L. V. Avioli

Interaction of calcium and phosphate decreases ileal magnesium solubility and apparent magnesium absorption in rats EJ Brink, AC Beynen, PR Dekker http://jn.nutrition.org/content/122/3/580.full.pdf

Calcium antagonizes magnesium in rats, but not in humans.

Acta Endocrinol (Copenh). 1977 Sep;86(1):81-8. Studies on circadian variations of plasma TSH, thyroxine and triiodothyronine in man. Lucke C, Hehrmann R, von Mayersbach K, von zur Mühlen A.

Free Radic Biol Med. 2000 Dec 15;29(12):1302-6. Hyperinsulinemia: the missing link among oxidative stress and age-related diseases? Facchini FS, Hua NW, Reaven GM, Stoohs RA.

Metabolism. 2002 Oct;51(10):1230-4. A calcium-deficient diet caused decreased bone mineral density and secondary elevation of estrogen in aged male rats-effect of menatetrenone and elcatonin. Kato S, Mano T, Kobayashi T, Yamazaki N, Himeno Y, Yamamoto K, Itoh M, Harada N, Nagasaka A.

Cardiovasc Diabetol. 2009 Feb 3;8:7. Parathyroid hormone, but not vitamin D, is associated with the metabolic syndrome in morbidly obese women and men: a cross-sectional study. Hjelmesaeth J, Hofsø D, Aasheim ET, Jenssen T, Moan J, Hager H, Røislien J, Bollerslev J. http://www.ncbi.nlm.nih.gov/pubmed/19187564

Arch Pharm Res. 2008 Jul;31(7):891-9. Epub 2008 Aug 14. Effects of calcium channel blockers on hyaluronidase-induced capillary vascular permeability. Halici Z, Suleyman H, Cadirci E.

Am J Clin Nutr. 2008 Oct;88(4):877-85. Dairy calcium supplementation in overweight or obese persons: its effect on markers of fat metabolism. Bortolotti M, Rudelle S, Schneiter P, Vidal H, Loizon E, Tappy L, Acheson KJ.

http://www.ncbi.nlm.nih.gov/pubmed/18842771

Dig Liver Dis. 2009 Aug;41(8):541-50. Epub 2009 Feb 4. Transglutaminases in inflammation and fibrosis of the gastrointestinal tract and the liver. Elli L, Bergamini CM, Bardella MT, Schuppan D.

Acta Endocrinol (Copenh). 1977 Sep;86(1):81-8. Studies on circadian variations of plasma TSH, thyroxine and triiodothyronine in man. Lucke C, Hehrmann R, von Mayersbach K, von zur Mühlen A. http://www.ncbi.nlm.nih.gov/pubmed/578614

Urinary Excretion of Calcium Following an Oral Calcium Loading Test in Healthy Children F. Bruder Stapleton, H. Norman Noe, Gerald Jerkins, Shane Roy III http://pediatrics.aappublications.org/content/69/5/594.short

http://www.nature.com/nrc/journal/v2/n4/full/nrc780.html http://www.nature.com/nrc/journal/v2/n4/full/nrc780.html

NF-B inhibitors might also prevent progression to colorectal cancer by preventing expression of COX2 — another NF-B target gene. COX2 is responsible for inducible prostaglandin synthesis during inflammation. The link between COX2 and colorectal cancer is supported strongly by epidemiological and experimental evidence. COX2 is overexpressed in colon adenomas and carcinomas of human and mouse origin89, 90, and Cox2-null mice are resistant to colorectal cancer91, 92. Long-term consumption of aspirin or other COX inhibitors over a period of 10–15 years has been reported to reduce the relative risk of colorectal cancer by 40–50% (Refs 93,94).

Given the ability of both aspirin and sulindac to inhibit IKK99, 100, it is possible that some of their chemopreventive activity is derived from their ability to prevent NF-B activation. Inhibition of IKK activity using sulindac sulphide was shown to induce the apoptosis of a colorectal cancer cell line100. Curcumin — another less potent and even less specific inhibitor of IKK — is another anti-inflammatory compound101. Curcumin has been shown to reduce colon carcinogenesis in several animal models95, 102 and to inhibit the proliferation of colon cancer cells103. Its extensive consumption in the Indian subcontinent has been linked to low incidence of colorectal cancer104

http://www.ncbi.nlm.nih.gov/pubmed/17622575 "By contrast, the anti-inflammatory effects of glucocorticoids are due largely to their ability to reduce the expression of pro-inflammatory genes. This effect has been predominantly attributed to the repression of key inflammatory transcription factors, including AP-1 and NF-kappaB, and is termed transrepression.

Physiol Behav. 1996 Jan;59(1):133-9. Nonsteroidal anti-inflammatory drugs alter body temperature and suppress melatonin in humans. Murphy PJ, Myers BL, Badia P.

ALDOSTERONE & AMMONIA

Aldosterone effects on renal metabolism. R S Snart and E Taylor http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1282502/

The dose-response characteristic obtained for this aldosterone-stimulated ammonia release has been determined. 4. The effect of a high Na+ diet on the ammonia release has been studied. An initial decrease after 2 days may be associated with decreased endogenous aldosterone secretion. However, aldosterone (2.5 microgram/100 g body weight)injections into these high Na+ treated animals fails to restore the normal ammonia release. 5. The effects of aldosterone (2.5 microgram/100 g body weight), dexamethasone (2.5 microgram/100 g body weight) and corticosterone (2.5 microgram/100 g body weight) injections, in adrenalectomized rats, on ammonia release and tissue tyrosine aminotransferase activities have been compared.

Antiinflammatory Action of Glucocorticoids — New Mechanisms for Old Drugs Turk Rhen, Ph.D., and John A. Cidlowski, Ph.D. N Engl J Med 2005; 353:1711-1723October 20, 2005 http://www.nejm.org/doi/full/10.1056/NEJMra050541

Am J Vet Res. 1978 Jan;39(1):159-61. Effect of thyroid state on magnesium concentration of rat tissues. Oliver JW.

Stimulatory effects of hyperprolactinemia on aldosterone secretion in ovariectomized rats. Kau MM, Chang LL, Kan SF, Ho LT, Wang PS. http://www.ncbi.nlm.nih.gov/pubmed/11928939

Metabolism. 2003 Aug;52(8):1072-7. Dietary sodium restriction exacerbates age-related changes in rat adipose tissue and liver lipogenesis. Xavier AR, Garófalo MA, Migliorini RH, Kettelhut IC.

Prog Lipid Res. 2000 May;39(3):231-55. Vitamin E: non-antioxidant roles. Azzi A, Stocker A.

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx Masafumi Zaitsu,a Shin-Ichiro Narita,a K. Chad Lambert,a James J. Grady,b D. Mark Estes,a Edward M. Curran,a Edward G. Brooks,a Cheryl S. Watson,c Randall M. Goldblum,a and Terumi Midoro-Horiutia* http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2603032/

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism. R C May, R A Kelly, and W E Mitch http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423396/

Regulation of GH Secretion in Acromegaly: Reproducibility of Daily GH Profiles and Attenuated Negative Feedback by IGF-I Craig A. Jaffe, Wenqin Pan, Morton B. Brown, Roberta DeMott-Friberg and Ariel L. Barkan http://jcem.endojournals.org/content/86/9/4364.full

Yet, nocturnal GH augmentation persisted during the infusion of a supraphysiological dose of octreotide, so that the nocturnal decline in somatostatin is unlikely to be the cause of the augmented GH secretion (32). Similarly, a nocturnal rise in GH secretion persisted despite continuous infusion of GH-releasing peptide-6 (33). This suggests that a nighttime increase in GH secretagogue is also unlikely to be the driving force for nocturnal GH release. In contrast, a continuous infusion of GHRH antagonist eliminated nearly all of the nocturnal GH rise in normal subjects (2). Therefore, the role of central GHRH as a driving force in normal and, conceivably, in acromegalic subjects needs to be considered.

Steroids. 1996 Apr;61(4):166-71. Effects of estrogens and progestogens on the renin-aldosterone system and blood pressure. Oelkers WK.

"Endogenous progesterone is a mineralocorticoid receptor antagonist. Endogenous or exogenous progesterone leads to sodium loss and a compensatory increase in renin secretion, plasma renin activity, AII, and plasma aldosterone, e.g. in the second half of the menstrual cycle.

Can J Physiol Pharmacol. 1982 Mar;60(3):331-4. Role of acidosis in the protein wasting of fasting in the rat and the rabbit. Hannaford MC, Goldstein MB, Josse RG, Halperin ML.

Steroids. 2005 May-Jun;70(5-7):347-51. Epub 2005 Mar 24. Nongenomic effects of mineralocorticoid receptor activation in the cardiovascular system. Mihailidou AS, Funder JW. http://www.ncbi.nlm.nih.gov/pubmed/15862816

In rabbit cardiomyocytes, aldosterone increases intracellular [Na+] by activating Na+/K+/2Cl- cotransport, with secondary effects on Na+/K+ pump activity. Pump current rises approximately 10-fold within 15', is unaffected by actinomycin D or the MR antagonist canrenone, and not elevated by cortisol. Pump current is, however, completely blocked by the open E-ring, water soluble MR antagonist K+ canrenoate and stoichometrically by cortisol.

Pathophysiology of hypertension during preeclampsia: linking placental ischemia with endothelial dysfunction Jeffrey S. Gilbert, Michael J. Ryan, Babbette B. LaMarca, Mona Sedeek, Sydney R. Murphy, and Joey P. Granger http://ajpheart.physiology.org/content/294/2/H541.full

"Studies from several laboratories indicate that chronic NO synthase inhibition in pregnant rats produces hypertension associated with peripheral and renal vasoconstriction, proteinuria, intrauterine growth restriction, and increased fetal morbidity (23, 43). We have previously reported similar cardiovascular perturbations exist in the NO inhibition and RUPP models, the latter illustrated in Fig. 2 (94).

http://ajpheart.physiology.org/content/294/3/H1258.full

Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension Rhian M. Touyz http://ajpheart.physiology.org/content/294/3/H1103.full

Aldosterone and end-organ damage Annis M. MARNEY and Nancy J. BROWN http://submit.clinsci.org/cs/113/0267/cs1130267.htm

, MR activation induces oxidative stress, endothelial dysfunction, inflammation and subsequent fibrosis.

Hypertension. 2004 Feb;43(2):358-63. Epub 2004 Jan 12. Epoxy-keto derivative of linoleic acid stimulates aldosterone secretion. Goodfriend TL, Ball DL, Egan BM, Campbell WB, Nithipatikom K. http://www.ncbi.nlm.nih.gov/pubmed/14718355?dopt=Abstract

Prog Cardiovasc Dis. 2010 Mar-Apr;52(5):401-9. Aldosterone: role in the cardiometabolic syndrome and resistant hypertension. Whaley-Connell A, Johnson MS, Sowers JR. http://www.ncbi.nlm.nih.gov/pubmed/14718355?dopt=Abstract

Review article Role of the renin–angiotensin–aldosterone system and inflammatory processes in the development and progression of diastolic dysfunction Sebastiano SCIARRETTA*, Francesco PANENI*, Francesca PALANO*, Diana CHIN*, Giuliano TOCCI*, Speranza RUBATTU*† and Massimo VOLPE*†

http://submit.clinsci.org/cs/116/0467/cs1160467.htm

Arterioscler Thromb Vasc Biol. 2002 Aug 1;22(8):1257-66. Vascular inflammation and the renin-angiotensin system. Brasier AR, Recinos A 3rd, Eledrisi MS. http://www.ncbi.nlm.nih.gov/pubmed/12171785

Brief Review Aldosterone and Vascular Inflammation Nancy J. Brown http://hyper.ahajournals.org/content/51/2/161.full

The role of oestrogen and progesterone receptors in hum www.biomedcentral.com/content/pdf/bcr452.pdf

Corticosteroids mediate fast feedback of the rat hypothalamic-pituitary-adrenal axis via the mineralocorticoid receptor Helen C. Atkinson, Susan A. Wood, Emma S. Castrique, Yvonne M. Kershaw, Crispin C. R. Wiles, and Stafford L. Lightman

J Nucleic Acids. 2010 Sep 22;2010. pii: 725071. Prevention of mutation, cancer, and other age-associated diseases by optimizing micronutrient intake. Ames BN. http://www.ncbi.nlm.nih.gov/pubmed/20936173

FASEB J. 2011 Jun;25(6):1793-814. Epub 2011 Mar 14. Adaptive dysfunction of selenoproteins from the perspective of the triage theory: why modest selenium deficiency may increase risk of diseases of aging. McCann JC, Ames BN.

Arther & Beckett. (1999) Thyroid function http://bmb.oxfordjournals.org/content/55/3/658.abstract?ijkey=142d514bc098871f0edbf58f0989a55060f2627a&keytype2=tf_ipsecsha

Arther & Beckett. (2004) Selenium and endocrine systems http://joe.endocrinology-journals.org/content/184/3/455.abstract?ijkey=62929d24abdd3d8eb6509950b387320efd616459&keytype2=tf_ipsecsha+html

Gut inflammation in chronic fatigue syndrome Shaheen E Lakhan* and Annette Kirchgessner http://www.nutritionandmetabolism.com/content/7/1/79/

Obesity and the human microbiome RE Ley http://bcrc.bio.umass.edu/courses/fall2010/biol/biolh100-01/sites/default/​files/​ley_microbiome_obesity_review_2010.pdf

Serum Ferritin Is Associated With Visceral Fat Area care.diabetesjournals.org/content/28/10/2486.full.pdf

Obesity, Visceral Fat, and NAFLD: Querying the Role of Adipokines in the Progression of Nonalcoholic Fatty Liver Disease M. S. Mirza http://www.isrn.com/isrn/gastroenterology/2011/592404/

Beneficial effects of enzyme-based therapy for autism spectrum disorders by Mark A. Brudnak, Bernard Rimland, Roy E. Kerry, Margaret Dailey, Robert Taylor, Bruce Stayton, Frank Waickman, Michael Waickman, Jon Pangborn, Ilene Buchholz

http://findarticles.com/p/articles/mi_m0ISW/is_243/ai_109946536/?tag=content;col1

Ann Allergy. 1994 May;72(5):462-8. Foods and additives are common causes of the attention deficit hyperactive disorder in children. Boris M, Mandel FS. http://calmglow.com/pdfs/food-allergies-and-ADHD.pdf

Do Artificial Food Colors Promote Hyperactivity in Children with Hyperactive Syndromes? A Meta-Analysis of Double-Blind Placebo-Controlled Trials http://www.cspinet.org/new/pdf/schab.pdf

The effects of a double blind, placebo controlled, artificial food colourings and benzoate preservative challenge on hyperactivity in a general population sample of preschool children B Bateman, J O Warner, E Hutchinson, T Dean, P Rowlandson, C Gant, J Grundy, C Fitzgerald, J Stevenson http://www.cspinet.org/new/pdf/bateman.pdf

Wednesday, November 9, 2011

The Best Way to Enlarge Your Penis

Your penis could grow larger through diet. But diet only helps so much. And even if your diet is optimal, your penis might still not grow as much. The only solution is to supplement.

The solution is to take supplements / herbs / drugs which boot your testosterone / DHT. Boosting your testosterone / DHT would make your penis grow larger.

There are "penis enlargement products." I have seen them, and they are basically vitamins/minerals/herbs which increase your testosterone / DHT levels. There is nothing special about them. If you increase your testosterone / DHT levels by other means, then it would have the same effect.

But do not take testosterone by itself. Taking testosterone by itself would, as a side-effect, increase your estradiol levels, as well. It might be harmful to take testosterone by itself, because taking testosterone increases estradiol, as well.

So you should increase your testosterone / DHT levels, without increasing your estradiol levels.

Also, a lot of the effects of those "penis enlargement products" are temporary. For instance, one of the ingredients in those products is called "l-arginine." L-arginine has been shown to increase the size of your penis. But the effect is temporary. All it does is that it dilates the blood vessels your penis, increasing the blood flow to your penis, thus making your penis look larger. And if you stop taking the l-arginine, your penis would shrink to the normal size. As you see, this is only a temporary effect.

Another ingredient in those "penis enlarge products" is Ginkgo biloba. But the effect is temporary as well. Ginkgo biloba only dilutes the blood vessels within the penis, thus increasing the blood flow to the penis, making it look bigger. But once you stop taking Ginkgo biloba, your penis would shrink. The effect is only temporary. So you should focus on permanently increasing your penis size, rather than just experiencing a temporary effect.

So you want a permanent effect on your penis growth. The only way to achieve a permanent effect is to raise your testosterone / DHT.

You could take some drugs / herbs / supplements / nutrients which could raise your testosterone / DHT production.

Some of those are:

  • Aspirin
  • Urtica dioica root (Nettle root)
  • Tribulus terrestris
  • Muira Puama
  • Zinc (be careful not to overdose.)
  • Vitamin A (be careful not to overdose. Get the retinol form.)

Aspirin, nettle root, and zinc function as "aromatase inhibitors." That is, they increase your testosterone levels by decreasing the conversion of testosterone to estrogen. So they could all increase your penis size, via increased testosterone and DHT.

If you look at the ingredients within those "penis enlargement products", then some of those actually lists maca root, saw palmetto, zinc, etc. Those "penis enlargement products" just combine some of those nutrients listed above, so you don't have to buy them separately.

But buying them separately is better. You could buy maca root and nettle root separately. And you could supplement with zinc separately. You don't have to take those "penis enlargement products." A lot of the ingredients have only a temporary effect. And a lot of the ingredients are harmful. Some of those ingredients have side effects which are toxic to the liver.

Here are some ingredients in those penis enlargement supplements:

  • Garlic - has been shown to be carcinogenic.
  • Ginseng - shown to be estrogenic.
  • Licorice - raises cortisol levels, and excess cortisol could speed up your rate of aging, and make you lose muscle mass.
  • l-arginine - raises nitric oxide production. But nitric oxide is a free radical. Excess nitric oxide causes aging, varicose veins, and edema.
  • Lepidium meyenii (Maca root) has indole-3-carbonal, which could increase your estradiol and decrease your androgen production.[9]
  • Saw palmetto inhibits 5-alpha reductase, which inhibits DHT and is anti-androgenic.
  • Epimedium sagittatum (Horny goat weed.) - raises estrogen levels

So I don't recommend buying those "penis enlargement products." I recommend supplementing some herbs/nutrients separately. Some of those ingredients could be obtained through diet, or supplementation if needed. Such as zinc and vitamin A.

REFERENCES

[1] Masterjohn, Chris. (2004). Vitamin A: The Forgotten Bodybuilding Nutrient

[2] Elements, Ed. (2010). Raising Testosterone Levels With Zinc Supplements and a High Zinc Diet

[3] Gansser D, Spiteller G. (1995). Aromatase inhibitors from Urtica dioica roots.

[4] Hartmann RW, Mark M, Soldati F. Inhibition of 5-alpha-reductase and aromatase by PHL-0081, a combination of PY102 (Pygeum africanum) and UR102 (Urtica dioica) extracts.

"Pygeum showed much higher efficacy at lower doses than did nettle root, but the combination of both herbs was significantly more effective than either alone in blocking the aromatase enzyme."

[5] Baiba J Grube3, Elizabeth T. Eng, Yeh-Chih Kao, Annette Kwon and Shiuan Chen. (2001). White Button Mushroom Phytochemicals Inhibit Aromatase Activity and Breast Cancer Cell Proliferation

[6] Hashida C, Hayashi K, Jie L, Haga S, Sakurai M, Shimizu H. (1990). [Quantities of agaritine in mushrooms (Agaricus bisporus) and the carcinogenicity of mushroom methanol extracts on the mouse bladder epithelium]

[7] Grube BJ, Eng ET, Kao YC, Kwon A, Chen S. (2001). White button mushroom phytochemicals inhibit aromatase activity and breast cancer cell proliferation.

[8] Chen S, Oh SR, Phung S, Hur G, Ye JJ, Kwok SL, Shrode GE, Belury M, Adams LS, Williams D. (2006). Anti-aromatase activity of phytochemicals in white button mushrooms (Agaricus bisporus).

[9] However, this claim is disputed by further studies. One study has shown that indol-3-carbonol lowers androgen levels. Another study has shown that it antagonize androgen levels in human prostate cancer cells. Therefore, one should be careful with supplementing with indol-3-carbonol, because it decreases androgen levels.

[10] Bovee TF, Schoonen WG, Hamers AR, Bento MJ, Peijnenburg AA. (2008) Screening of synthetic and plant-derived compounds for (anti)estrogenic and (anti)androgenic activities.

"3,3'-diindolylmethane (DIM) and equol combined an estrogenic mode of action with an antiandrogenic activity. Indol-3-carbinol (I3C) only showed an antiandrogenic activity."

[11] Hien T. Le, Charlene M. Schaldach, Gary L. Firestone and Leonard F. Bjeldanes. (2003). Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells

[12] Zhang CZ et al. In vitro estrogenic activities of Chinese medicinal plants traditionally used for the management of menopausal symptoms. Journal of Ethnopharmacology. 98.3 (2005):295-300.

[13] Pygeum (Prunus africanum, Pygeum africanum)

Traits which Women Find Attractive in a Man

There are a lot of things that a woman find in a man attractive. Women are attracted to dominance, social status, confidence, ruggedness, height, a "strong" face, broad shoulders, muscles, body hair, large hands and feet, etc.

Social status is big for women. Women are also attracted to men who play "hard-to-get." And there are yet other features which women are attracted to. Women are attracted to men who are dominant. They are attracted to men who are leaders. They are attracted to men who are the "center of the attention."

Do you know why so many women are attracted to doctors, lawyers, businessmen, and cops? Because they have "authority." People look up to them, pay attention to them, listen to them, and learn from them. They are very attractive to women.

Fame is also attractive to women. Famous people such as actors, singers, and athletes are very attractive to women. Do you know why? Because fame is a sign of status. Imagine an actor who is in a movie. People watch the movie. People pay attention to the actor. It's like the actor being the "center of attention." Women are attracted to celebrities because they receive a lot of attention from people. It's a sign of authority.

I'm not saying that a man who tries too hard to *seek* attention is attractive. That's not. What I'm saying is the men who *receive* a lot of attention from others will be attractive.

Voice is a big thing that a woman will notice. Do you wonder why do those male singers get all the women? Do you wonder why a lot of women scream and cheer at concerts? Why do so many women have crushes on famous singers? Well, one factor is that those men have an attractive voice. Women are attracted to that. It's big. A deep, confident, and resonating voice is very attractive to women. That alone can make an average man very attractive to women.

But a lot of male singers have high-pitched, whiny voices. Why do they still attract a lot of women? Let's look at the positives. They're already famous, so their fame in itself will attract a lot of women. Besides fame, those men's voices are confident and resonating. They know how to tune the timing of their words, to make their voice sound confident. They sing loudly, which is also a sign of confidence. They use their diaphragm to make their voice resonate. A resonating voice is yet another sign of confidence.

Another thing which is attractive to male singers is "pre-selection." Pre-selection is a theory that a male will become more attractive if other women are also attracted to him. Famous male singers usually have millions of women going crazy for them, and that, in itself, would make them even more attractive to those women. And do you know why a lot of women are attracted to "taken" or "married" men? One of the reasons that those men are pre-selected by their girlfriends / wives.

There are other features which women find attractive. They are attracted to risk-taking men. Men who risk their lives are very attractive to women. A lot of women are attracted to firefighters, because they are risk-taking. Similarly, women are attracted to rugged, sporty men. And women are attracted to rich men, and men who dress like rich men. (i.e. Don't dress like a bum. Wear clothes which are tailored, clean, ironed, and fashionable.)

Body odor is huge. Pheromones are huge. The major histocompatibility complex (MHC) is huge factor in sex appeal, as well.

References

[1] Pheromone articles

[2] There's a whole community out there about men wearing commercial pheromone colognes to attract women. (www.pheromonetalk.com) Those commercial pheromone colognes seem to work for men, though there isn't solid evidence. It's based on their grossly inaccurate observations. (i.e. "a woman looked at me; she must be attracted to me", "a woman smiled at me, she must be attracted to me", or "a woman chatted with me; she must be attracted to me." - not to mention placebo effects)