The Paleolithic period represents just the last two million years of human evolution. What did our bodies evolve to eat during the first 90% of our time on Earth? A folic acid test measures the amount of folic acid in the blood. Folic acid is one of many B vitamins. The body needs folic acid to make red blood cells (RBC), white. 23andMe is the first and only genetic service available directly to you that includes reports that meet FDA standards. Low Histamine Diet & Histamine Intolerance. One-quarter of what you eat keeps you alive. The other three-quarters keep your doctor alive. Maximizing Methylation: The Key to Healthy Aging. TAKING JUST A FEW vitamins CAN optimize the function of ALL your body’s systems. But you have to know what to take and you have to know why these supplements work . In today’s blog I will review the 8 factors that can lead to problems in this area, and outline 1. But first, I’d like to tell you about two of my patients with seemingly unrelated health problems that were actually caused by a breakdown in this biochemical process. ![]() ![]() And I want to share a study done on Chinese babies who had a birth defect known as spina bifida. You’ll be amazed at how all three — my two patients and these Chinese babies — were affected by the exact same thing . Roberts, and Mr. Mc. Nally all have something very important in common. They all have inadequate levels of specific vitamins, either acquired or genetic, . Roberts, was an 8. He still golfed three times a week, worked two days a week, flew around the world in his private jet, and was “romantic” once a week with a wife 3. He also loved his 6 ounces of Grey Goose vodka every night. Of course, he did have some health problems. Roberts had been treated well for mild heart disease. His doctor even recommended 8. B1. 2 — megadoses by any standard. Mr. Roberts also had a check- up at the Mayo Clinic and was told that he was healthy, despite having mild anemia and large red blood cells. Yet he still complained of mild fatigue and trouble with his short- term memory. Plus, I noticed a slightly wide gait common in someone with poor balance. Then there was Mr. Mc. Nally, a Boston college professor who was 5. He recounted the sad tale of his 7 brothers. Four had died of a heart attack and three others had had bypass operations at a young age. Concerned about his own fate, he ate a low- fat diet, exercised regularly, didn’t smoke, had normal blood pressure and cholesterol levels, and took antioxidants and a multivitamin. Perhaps his only vice was the multiple Starbuck’s grande lattes he downed each day. Living under a constant state of impending doom, Mr. MTHFR.net is the leading resource for unbiased, researched information strictly about the MTHFR mutation. I believe the MTHFR gene mutation is a highly significant. Mc. Nally came to me asking for a stress test to see how his heart was doing. Strange as it may seem, these two men reminded me of my time in China. When I lived in Beijing, a study was done on a group of women in Harbin, the northern most industrial city in the Gobi desert, just north of Beijing. It seemed that there was an unusually high rate of birth defects in the area, specifically spina bifida. The Chinese have a tradition of holding weddings during the Chinese New Year in February. In Harbin, many of the babies born 9 months later had birth defects. This study sought to determine what the link was and found that the major factor was the lack of fresh greens or vegetables in the Gobi desert in the middle of winter. ![]() Interestingly, these Chinese babies, Mr. Roberts, and Mr. Mc. Nally all have something very important in common. They all have inadequate levels of specific vitamins, either acquired or genetic, and their methylation systems are not working properly as a result. I’ll explain more about what “methylation” is in a second. First let’s analyze the similarities in these cases. Take Mr. Our romantically active 8. B vitamins. But he still had very high levels of homocysteine and methylmalonic acid — indicators of folic acid and B1. Mr. Mc. Nally had similar problems. Our college professor had a genetically sluggish metabolism of homocysteine which caused extremely high levels of this toxic amino acid to build up in his blood. This was the likely cause of all the heart disease in his family. Again we see a similar set of problems in those Chinese babies. Their mothers were conceiving in the middle of winter — when their folate intake was low from the absence of fruits and vegetables. This is what triggered such a high rate of birth defects. The common link in all three of these cases is a problem with methylation. Let me tell you more about that that actually means. Methylation is a key biochemical process that is essential for the proper function of almost all of your body’s systems. It occurs billions of times every second; it helps repair your DNA on a daily basis; it controls homocysteine (an unhealthy compound that can damage blood vessels); it helps recycle molecules needed for detoxification; and it helps maintain mood and keep inflammation in check. To keep methylation running smoothly you need optimal levels of B vitamins. Without enough B vitamins methylation breaks down, and the results can be catastrophic. In these cases we see more birth defects like spina bifida (as with the Chinese babies), more cases of Down’s syndrome, and more miscarriage. A breakdown in methylation also puts you at higher risk for conditions like osteoporosis, diabetes, cervical dysplasia and cancer, colon cancer, lung cancer, depression, pediatric cognitive dysfunction ( mood and other behavioral disorders), dementia, and stroke. And like Mr. Roberts and Mr. Mc. Nally, you may be at higher risk for cardiovascular disease. To avoid all of these problems, the key is to maximize methylation. That means avoiding the things that cause your methylation to break down, testing to find out how well your methylation is working, and including the things that support proper methylation. Let’s look at how to do that. Factors that Affect Your Methylation Process. Genetics – Like an estimated 2. Poor diet – The word “folate” comes from “foliage.” You need to eat plenty of leafy greens, beans, fruit, and whole grains to get adequate levels of vitamins B6 and B1. Egg yolks, meat, liver, and oily fish are the main dietary sources of vitamin B1. Plus, certain compounds can raise levels of homocysteine and deplete the B vitamins. These include excess animal protein, sugar, saturated fat, coffee, and alcohol. Irradiation of food depletes nutrients, so foods treated this way may be lower in B vitamins, too. Smoking – The carbon monoxide from cigarette smoke inactivates vitamin B6. Malabsorption – Conditions like digestive diseases, food allergies, and even aging can reduce absorption of nutrients. Decreased stomach acid – Aging and other conditions can reduce stomach acid — and therefore absorption of vitamin B1. Medications – Drugs like acid blockers, methotrexate (for cancer and arthritis and other autoimmune diseases), oral contraceptives, HCTZ (for high blood pressure), and Dilantin (for seizures) can all affect levels of B vitamins. Other conditions – These include hypothyroidism, kidney failure or having only one kidney, cancer, and pregnancy. Toxic exposures – Some toxins can interfere with vitamin production. Watch out for these factors and you will go a long way toward protecting your methylation. Measuring Your Own Methylation Process. To find out if your methylation process is optimal, ask your doctor for the following tests: Complete blood count – Like our friend Mr. Roberts, large red blood cells or anemia can be a sign of poor methylation. Red blood cells with a mean corpuscular volume (MCV) greater than 9. Homocysteine – This is one of the most important tests you can ask for. The normal level is less than 1. Serum or urinary methylmalonic acid – This is a more specific test for vitamin B1. Your levels may be elevated even if you have a normal serum vitamin B1. Specific urinary amino acids – These can be used to look for unusual metabolism disorders involving vitamins B6 or B1. Tips to Optimize Your Methylation Process. Just as there are many causes of poor methylation, there are lots of things that support its proper functioning. Here’s how to maximize methylation — and prevent conditions like heart disease, cancer, dementia, depression, and more. Eat more dark, leafy greens – You want to eat l cup a day of vegetables like bok choy, escarole, Swiss chard, kale, watercress, spinach, or dandelion, mustard, collard, or beet greens. These are among the most abundant sources of the nutrients needed for optimal methylation. Get more Bs in your diet – Good food sources include sunflower seeds and wheat germ (vitamin B6); fish and eggs (vitamin B6 and B1. B1. 2); beans and walnuts (vitamin B6 and folate); leafy dark green vegetables; asparagus, almonds, and whole grains (folate); and liver (all three)Minimize animal protein, sugar, and saturated fat – Animal protein directly increases homocysteine. Sugar and saturated fat deplete your body’s vitamin stores. Avoid processed foods and canned foods – These are depleted in vitamins. Avoid caffeine – Excess amounts can deplete your B vitamin levels. Limit alcohol to 3 drinks a week – More than this can deplete your B vitamin levels. Don’t smoke – As noted above, smoking inactivates vitamin B6. Avoid medications that interfere with methylation – See notes on this above. Keep the bacteria in your gut healthy – Take probiotic supplements and use other measures to make sure the bacteria in your gut are healthy so you can properly absorb the vitamins you do get. Improve stomach acid – Use herbal digestives (bitters) or taking supplemental HCl. Take supplements that prevent damage from homocysteine – Antioxidants protect you from homocysteine damage. Also make sure you support methylation with supplements like magnesium and zinc. Supplement to help support proper homocysteine metabolism – Talk to your doctor to determine the best doses and forms for you. Some people may also need to take preformed folate (folinic acid or 5 formyl. THF) to bypass some of the steps in activating folic acid. Vitamin B6: Take 2 to 5 mg a day. Some people may need up to 2. B6 (pyridoxyl- 5- phosphate) to achieve the greatest effect. Doses higher than 5. Vitamin B1. 2: Doses of 5. Oral vitamin B1. 2 isn’t well absorbed; you may need up to 1 or 2 mg daily. Ask your doctor about B1. Betaine: This amino acid derivative is needed in doses from 5. By working to optimize your methylation you can protect yourself from virtually all the so called “diseases of aging.” When you do, you will be well on the road to lifelong vibrant health. Now I’d like to hear from you ? Have you noticed any results? Anabolic steroid - Wikipedia. This article is about androgens as medications. For androgens as natural hormones, see Androgen. Anabolic steroids, also known more properly as anabolic- androgenic steroids (AAS). They are anabolic and increase protein within cells, especially in skeletal muscles. AAS also have varying degrees of androgenic and virilizing effects, including induction of the development and maintenance of masculinesecondary sexual characteristics such as the growth of the vocal cords and body hair. The word anabolic, referring to anabolism, comes from the Greek . The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight, often as lean mass increases and that the gains in muscular strength achieved through high- intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals. Their use is referred to as doping and banned by most major sporting bodies. For many years, AAS have been by far the most detected doping substances in IOC- accredited laboratories. Testosterone is now nearly the only androgen used for this purpose and has been shown to increase height, weight, and fat- free mass in boys with delayed puberty. These sports include bodybuilding, weightlifting, shot put and other track and field, cycling, baseball, wrestling, mixed martial arts, boxing, football, and cricket. Such use is prohibited by the rules of the governing bodies of most sports. AAS use occurs among adolescents, especially by those participating in competitive sports. It has been suggested that the prevalence of use among high- school students in the U. S. Oral administration is the most convenient. Testosterone administered by mouth is rapidly absorbed, but it is largely converted to inactive metabolites, and only about 1/6 is available in active form. In order to be sufficiently active when given by mouth, testosterone derivatives are alkylated at the 1. This modification reduces the liver's ability to break down these compounds before they reach the systemic circulation. Testosterone can be administered parenterally, but it has more irregular prolonged absorption time and greater activity in muscle in enanthate, undecanoate, or cypionateester form. These derivatives are hydrolyzed to release free testosterone at the site of injection; absorption rate (and thus injection schedule) varies among different esters, but medical injections are normally done anywhere between semi- weekly to once every 1. A more frequent schedule may be desirable in order to maintain a more constant level of hormone in the system. In addition, because estered testosterone is dissolved in oil, intravenous injection has the potential to cause a dangerous embolism (clot) in the bloodstream. Transdermal patches (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream. Testosterone- containing creams and gels that are applied daily to the skin are also available, but absorption is inefficient (roughly 1. Individuals who are especially physically active and/or bathe often may not be good candidates, since the medication can be washed off and may take up to six hours to be fully absorbed. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose himself or herself; children and women are highly sensitive to testosterone and can suffer unintended masculinization and health effects, even from small doses. Injection is the most common method used by individuals administering AAS for non- medical purposes. Studies indicate that the anabolic properties of AAS are relatively similar despite the differences in pharmacokinetic principles such as first- pass metabolism. However, the orally available forms of AAS may cause liver damage in high doses. AAS were ranked 1. Long- term steroid abusers may develop symptoms of dependence and withdrawal on discontinuation of AAS. Recreational AAS use appears to be associated with a range of potentially prolonged psychiatric effects, including dependence syndromes, mood disorders, and progression to other forms of substance abuse, but the prevalence and severity of these various effects remains poorly understood. As a result, AAS users may get misdiagnosed by a psychiatrist not told about their habit. Case reports describe both hypomania and mania, along with irritability, elation, recklessness, racing thoughts and feelings of power and invincibility that did not meet the criteria for mania/hypomania. Compared with individuals that did not use steroids, young adult males that used AAS reported greater involvement in violent behaviors even after controlling for the effects of key demographic variables, previous violent behavior, and polydrug use. The drug response was highly variable. However: 8. 4% of subjects exhibited minimal psychiatric effects, 1. The mechanism of these variable reactions could not be explained by demographic, psychological, laboratory, or physiological measures. There have been anecdotal reports of depression and suicide in teenage steroid users. A 1. 99. 2 review found that AAS may both relieve and cause depression, and that cessation or diminished use of AAS may also result in depression, but called for additional studies due to disparate data. Most of these side- effects are dose- dependent, the most common being elevated blood pressure, especially in those with pre- existing hypertension. For example, AAS may prematurely stop the lengthening of bones (premature epiphyseal fusion through increased levels of estrogen metabolites), resulting in stunted growth. Other effects include, but are not limited to, accelerated bone maturation, increased frequency and duration of erections, and premature sexual development. AAS use in adolescence is also correlated with poorer attitudes related to health. Development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase. This side- effect is temporary; the size of the testicles usually returns to normal within a few weeks of discontinuing AAS use as normal production of sperm resumes. Alteration of fertility and ovarian cysts can also occur in females. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe. Water- soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction with the cell’s surface receptors. However, as fat- soluble hormones, AAS are membrane- permeable and influence the nucleus of cells by direct action. The pharmacodynamic action of AAS begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor (AR) located in the cytoplasm of that cell. From there, the compound hormone- receptor diffuses into the nucleus, where it either alters the expression of genes. It has been hypothesized that this reduction in muscle breakdown may occur through AAS inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles. Through a number of mechanisms AAS stimulate the formation of muscle cells and hence cause an increase in the size of skeletal muscles, leading to increased strength. Depending on the length of use, the side effects of the steroid can be irreversible. Processes affected include pubertal growth, sebaceous gland oil production, and sexuality (especially in fetal development). Some examples of virilizing effects are growth of the clitoris in females and the penis in male children (the adult penis size does not change due to steroids. Men may develop an enlargement of breast tissue, known as gynecomastia, testicular atrophy, and a reduced sperm count. Compounds with a high ratio of androgenic to an anabolic effects are the drug of choice in androgen- replacement therapy (e. Determination of androgenic: anabolic ratio is typically performed in animal studies, which has led to the marketing of some compounds claimed to have anabolic activity with weak androgenic effects. This disassociation is less marked in humans, where all AAS have significant androgenic effects. The VP weight is an indicator of the androgenic effect, while the LA weight is an indicator of the anabolic effect. Two or more batches of rats are castrated and given no treatment and respectively some AAS of interest. The LA/VP ratio for an AAS is calculated as the ratio of LA/VP weight gains produced by the treatment with that compound using castrated but untreated rats as baseline: (LAc,t–LAc)/(VPc,t–VPc). The LA/VP weight gain ratio from rat experiments is not unitary for testosterone (typically 0. AAS, which have their androgenic: anabolic ratios scaled accordingly (as shown in the table above). Animal studies also found that fat mass was reduced, but most studies in humans failed to elucidate significant fat mass decrements. The effects on lean body mass have been shown to be dose- dependent. Both muscle hypertrophy and the formation of new muscle fibers have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out. After drug withdrawal, the effects fade away slowly, but may persist for more than 6–1. AAS use. Overall, the exercise where the most significant improvements were observed is the bench press. AR agonists are antigonadotropic – that is, they dose- dependently suppress gonadal testosterone production and hence reduce systemic testosterone concentrations.
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