back on track
Since my mother’s heart attack in march of 2010, and my adventure a day after they released her, I’ve been trying to keep my act together health wise.
I’ve been doing a 5 mile fast walk most days, with the intent of keeping my heart rate up for at least 45 minutes, as I try to keep in compliance with the 200 minutes of exercise a week (or better) rule.
I’ve got a nice route I do, lots of things to see and quite varied terrain.
The first mile of it is all downhill, (can’t be helped because of where I live) which sounds nice and easy, but that means the last mile is all uphill. 🙁
To be honest, I miss my roller skates. I’ve considered getting outdoor wheels for them, but quads and Washington weather don’t really work well together.
Generally it’s been working. I’ve still got a sysadmin belly, which I blame on fast food and soda, but I’ve got my wind back and I physically feel better.
I’ve had a lot of major upheavals in my life recently, completely derailing the balance of health, wealth, and relationships, that one needs to have to be happy.
The past 8 months have been very hard, mostly due to events beyond my control, and the sheer amount of stress that I’ve been dealing with for the past couple years.
Major Depression, lack of sleep, inability to focus, just to name a few.
Considering who I am and the kind of things I do, this is a really bad sign.
I was taking these supplements:
Spring Valley, Enteric Coated, Fish Oil. (3600mg a day, 1080mg a day of omega 3)
Fish oil has been studied for treating clinical depression, anxiety, and high blood pressure.
Countries with the highest intake of fish in their diets are correlated with the lowest rates of depression among citizens.
Several studies report possible anti-cancer effects of n−3 fatty acids found in fish oil (particularly breast, colon and prostate cancer).
Omega-3 fatty acids reduced prostate cancer growth, slowed histopathological progression, and increased survival in genetically engineered mice.
Among n-3 fatty acids (omega-3), neither long-chain nor short-chain forms were consistently associated with breast cancer risk.
High levels of docosahexaenoic acid, however, the most abundant n-3 polyunsaturated fatty acid (omega-3) in erythrocyte membranes, were associated with a reduced risk of breast cancer.
In a recent study of 35,000 middle-aged women published in the journal Cancer Epidemiology, those that took fish oil supplements were found to have a 32% lower risk of breast cancer, although the study authors stressed that the result was preliminary and that “we should not draw any conclusions about a causal relationship.”
The US National Institutes of Health lists three conditions for which fish oil and other omega-3 sources are most highly recommended: hypertriglyceridemia, secondary cardiovascular disease prevention and high blood pressure. It then lists 27 other conditions for which there is less evidence. It also lists possible safety concerns: “Intake of 3 grams per day or greater of omega-3 fatty acids may increase the risk of bleeding, although there is little evidence of significant bleeding risk at lower doses. Very large intakes of fish oil/omega-3 fatty acids may increase the risk of hemorrhagic (bleeding) stroke.”
Studies published in 2004 and 2009 have suggested that fish oil may reduce the risk of depression and suicide. One such study took blood samples of 100 suicide-attempt patients and compared the blood samples to those of controls and found that levels of Eicosapentaenoic acid were significantly lower in the washed red blood cells of the suicide-attempt patients. A small American trial, published in 2009, suggests that E-EPA, as monotherapy, might treat major depressive disorder, however the study achieved no statistical significance.
According to a study from Louisiana State University in September 2005, fish oil may help protect the brain from cognitive problems associated with Alzheimer’s disease.
A study examining whether omega-3 exerts neuroprotective action in Parkinson’s disease found that it did, using an experimental model, exhibit a protective effect (much like it did for Alzheimer’s disease as well). The scientists exposed mice to either a control or a high omega-3 diet from two to twelve months of age and then treated them with a neurotoxin commonly used as an experimental model for Parkinson’s. The scientists found that high doses of omega-3 given to the experimental group completely prevented the neurotoxin-induced decrease of dopamine that ordinarily occurs. Since Parkinson’s is a disease caused by disruption of the dopamine system, this protective effect exhibited could show promise for future research in the prevention of Parkinson’s disease.
Evidence regarding the efficacy of fish oil supplements as a treatment for depression is currently inconclusive. Whereas several methodologically rigorous studies have reported statistically significant positive effects in the treatment of depressed patients, other studies have found effects to be small or insignificant.
For example, an August 2003 double-blind placebo-controlled study published in the journal European Neuropsychopharmacology found that among 28 patients with major depressive disorder, “patients in the omega-3 PUFA group had a significantly decreased score on the 21-item Hamilton Rating Scale for Depression than those in the placebo group.” Another study in the American Journal of Psychiatry reported that the addition of fish oil supplements to regular maintenance anti-depression therapy conferred “highly significant” benefits by the third week of the trial.
Despite the conflicting scientific evidence for the efficacy of fish oil in treating depression, web searches reveal a large amount of anecdotal evidence for its alleged benefits. Notably, it does not appear that any peer-reviewed studies have reported negative effects on depressive symptoms as a result of fish oil supplementation.
Spring Valley High Potency B Complex (one per day, in the morning)
Promotes energy and metabolism.
Recommended as part of daily regimen for health, stress, mood, and energy.
Vitamin B-6 builds body proteins; riboflavin and niacin regulate antioxidant activity.
Specially formulated to replenish the nutrients lost during high stress times.
Vitamin B-1 (Thiamin Mononitrate) 50mg
Vitamin B-2 (Riboflavin) 12.5mg
Vitamin B-3 (Niacinamide) 50mg
Vitamin B-6 (Pyridoxine Hydrochloride) 12.5mg
Folate (Folic Acid) 50mcg
Vitamin B-12 (Cyanocobalamin) 12.5mcg
Pantothenic Acid (d-Calcium Pantothenate) 50mg
Calcium (Dicalcium Phosphate) 118mg
The Vitamin B Complex comprises of the essential B Vitamins – Vitamin B1, Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B6, Vitamin B9, Vitamin B12 plus the vitamins Biotin, Choline and Inositol. Vitamin B Complex is needed for the proper functioning of almost every process in the body.
Vitamin B1 is needed to help convert the carbohydrates we eat into glucose. The following B Vitamins are needed at a cellular level to convert glucose into energy – Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B6 and Biotin. A Vitamin B deficiency in any of these vitamins can lead to decreased energy production, lethargy and fatigue.
Healthy Nervous system
The Vitamin B Complex is essential for the healthy functioning of the nervous system. Vitamin B5 is needed for the correct functioning of the adrenal glands and the production of some hormones and nerve regulating substances. Vitamin B1, Vitamin B6 and Vitamin B12 are essential for the regulation and correct functioning of the entire nervous
system including brain function. Vitamin B9 is essential to prevent neural tube defects to the foetus during pregnancy. A deficiency in any of the Vitamin B Complex vitamins can lead to feeling stressed, anxious and depressed.
The Vitamin B Complex is essential for correct digestion, production of HCl (Hydrochloric acid) and to assist in the breakdown of fats, proteins and carbohydrates. Especially vital for good digestion are Vitamin B1, Vitamin B2, Vitamin B3 and Vitamin B6. A deficiency in any of these B Vitamins can lead to impaired digestion and deficiency of essential nutrients.
Healthy Skin, Hair and Nails
The Vitamin B Complex is essential for correct RNA and DNA synthesis and cell reproduction. As our Skin, Hair and Nails are constantly growing and renewing themselves we need the following B vitamins to ensure the good health of these structures – Vitamin B1, Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B9, Vitamin B12, Biotin and Choline. Deficiencies of any of these B Vitamins can lead to dry, grey skin, dermatitis, wrinkles, acne, rashes, falling hair and weak, splitting nails.
They were working pretty well for me, so I started taking them when I climbed back in the saddle so to speak.
Thing is, I couldn’t break the depression cycle, and the “spent 3 days in bed because I’m too depressed to do anything” thing really had to stop…
So after much research, I went shopping today and picked up the following supplements:
Natural Balance “happy camper” herbal formula (one per day, in the morning)
A couple friends of mine swear by this stuff, so I figured I would try it.
Basically, it’s a proprietary blend of:
Passion Flower (aerial portion extract)
(helps relieve tension and complements the action of Kava Kava)
Kava Kava (root, rhizome)
(produces a pleasant, cheerful, and sociable feeling while helping to reduce anxiety)
(builds resistance to stress and fatigue)
Gotu Kola (aerial portion extract)
(calms the brain, enhances mental clarity, and helps the body adapt to stress)
Kola Nut (seed extract contains caffeine)
(cardiac and central-nervous-system stimulant)
(brightens the mind )
Wood Betony (aerial portion)
(feeds and strengthens the nervous system)
(removes nervous tension)
NOW Mood Support With St. John’s Wort. (one per day in the morning)
“Mood Support is a nutritional supplement that contains both nutrients and herbal extracts that aid in the support of a healthy nervous system and a positive, balanced mood state.”
Mood Support contains:
Thiamine (from Thiamine HCl) (Vitamin B-1) 4mg
Niacin (as Niacinamide) (Vitamin B-3) 25mg
Vitamin B-6 (from Pyridoxine HCl) 10mg
Folate (Folic Acid) 400mcg
Vitamin B-12 (as Cyanocobalamin) 200mcg
Pantothenic Acid (from D-Calcium Pantothenate) 50mg
Magnesium (from Magnesium Oxide and Amino Acid Chelate) 50mg
Zinc (from Zinc L-Methionine) 5mg
Manganese (from Manganese Amino Acid Chelate) 2mg
St. John’s Wort Extract (Hypericum perforatum) (Aerial Part with Flowers) (min. 0.3% Hypericin) 450mg
Holy Basil Extract (Tuisi Extract) (Leaves) (Ocimum tenuiflorum) (min. 2% Ursolic Acid) 100mg
Valerian 4:1 Extract (Valeriana officinalis) (Root) 50mg
5-HTP (5-hydroxytryptophan) (Griffonia simplicifolia) (Seed) 20mg
GABA (Gamma Aminobutyric Acid) (Free-Form) 250mg
Taurine (Free-Form) 125mg
L-Theanine (Suntheanine®) 50mg
Note that this adds a substantial amount of B complex, but it is *very* hard to overdose on B complex, as they are all water soluble. This means excess vitamins are expelled in the urine. I don’t know anyone willing to take 30 high potency b complex tablets at once, but, that’s what it takes to “overdose” and the only result would be bright yellow urine. So, while you can od on B complex, its only dangerous in people who are already allergic to one of the B vitamins.
This works very well in conjunction with the “Happy Camper” mentioned above.
NOW Melatonin (one per day, taken at bedtime)
Melatonin is a naturally occurring hormone produced by the pineal gland that plays a role in the regulation of the sleep-wake cycle. The pineal is embedded in the brain and receives signals via the optic nerve. Melatonin is secreted by the gland after the body senses darkness at the end of each day to keep our bodies synchronized with the rhythms of day and night. Melatonin is often used as a home remedy for jet lag.
Dietary tryptophan is converted to 5-HTP, which in turn can convert to serotonin and then to melatonin. People with diets low in tryptophan or who lack darkness at night may have a functional deficit of serotonin and melatonin, making melatonin supplementation useful.
Melatonin is also a powerful antioxidant that supports immune system function and is an antagonist to cortisol, the stress hormone produced by the adrenal glands. Cortisol is partly responsible for many of the classic symptoms of chronic stress, including lack of sleep.
Human melatonin production decreases as a person ages.
Production of melatonin by the pineal gland is inhibited by light and permitted by darkness. For this reason melatonin has been called “the hormone of darkness”. Its onset each evening is called the Dim-Light Melatonin Onset (DLMO). Secretion of melatonin as well as its level in the blood, peaks in the middle of the night, and gradually falls during the second half of the night, with normal variations in timing according to an individual’s chronotype. Terman et al. devised a formulation which mimics that gradual washout (vs. the spikes in blood concentration and rapid washout associated with most over-the-counter melatonin tablets). When used several hours before sleep, the compound shifts the circadian clock earlier, thus promoting earlier sleep onset and morning awakening.
Besides its function as synchronizer of the biological clock, melatonin also exerts a powerful antioxidant activity. The discovery of melatonin as an antioxidant was made in 1993. In many less complex life forms, this is its only known purpose. Melatonin is an antioxidant that can easily cross cell membranes and the blood-brain barrier. Melatonin is a direct scavenger of OH, O2-, and NO. Unlike other antioxidants, melatonin does not undergo redox cycling, the ability of a molecule to undergo reduction and oxidation repeatedly. Redox cycling may allow other antioxidants (such as vitamin C) to act as pro-oxidants, counter intuitively promoting free radical formation. Melatonin, on the other hand, once oxidized, cannot be reduced to its former state because it forms several stable end-products upon reacting with free radicals. Therefore, it has been referred to as a terminal (or suicidal) antioxidant.
Recent research indicates that the first metabolite of melatonin in the melatonin antioxidant pathway may be N(1)-acetyl-N(2)-formyl-5-methoxykynuramine (or AFMK) rather than the common, excreted 6-hydroxymelatonin sulfate. AFMK alone is detectable in unicellular organisms and metazoans. A single AFMK molecule can neutralize up to 10 ROS/RNS (reactive oxygen species/reactive nitrogen species) since many of the products of the reaction/derivatives (including melatonin) are themselves antioxidants. This capacity to absorb free radicals extends at least to the quaternary metabolites of melatonin, a process referred to as “the free radical scavenging cascade”. This is not true of other, conventional antioxidants.
In animal models, melatonin has been demonstrated to prevent the damage to DNA by some carcinogens, stopping the mechanism by which they cause cancer. It also has been found to be effective in protecting against brain injury caused by ROS release in experimental hypoxic brain damage in newborn rats. Melatonin’s antioxidant activity may reduce damage caused by some types of Parkinson’s disease, may play a role in preventing cardiac arrhythmia and may increase longevity; it has been shown to increase the average life span of mice by 20% in some studies.
While it is known that melatonin interacts with the immune system, the details of those interactions are unclear. There have been few trials designed to judge the effectiveness of melatonin in disease treatment. Most existing data are based on small, incomplete clinical trials. Any positive immunological effect is thought to result from melatonin acting on high affinity receptors (MT1 and MT2) expressed in immunocompetent cells. In preclinical studies, melatonin may enhance cytokine production, and by doing this counteract acquired immunodeficiences. Some studies also suggest that melatonin might be useful fighting infectious disease including viral, such as HIV, and bacterial infections, and potentially in the treatment of cancer.
Endogenous melatonin in human lymphocytes has been related to interleukin-2 (IL-2) production and to the expression of IL-2 receptor. This suggests that melatonin is involved in the clonal expansion of antigen-stimulated human T lymphocytes. When taken in conjunction with calcium, it is an immunostimulator and is used as an adjuvant in some clinical protocols; conversely, the increased immune system activity may aggravate autoimmune disorders. In rheumatoid arthritis patients, melatonin production has been found increased when compared to age-matched healthy controls.
Some supplemental melatonin users report an increase in vivid dreaming. Extremely high doses of melatonin (50 mg) dramatically increased REM sleep time and dream activity in both people with and without narcolepsy. Many psychoactive drugs, such as cannabis and lysergic acid diethylamide (LSD), increase melatonin synthesis. It has been suggested that nonpolar (lipid-soluble) indolic hallucinogenic drugs emulate melatonin activity in the awakened state and that both act on the same areas of the brain.
Individuals with autism spectrum disorders (ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis.
Current and potential medical indications
Melatonin has been studied for the treatment of cancer, immune disorders, cardiovascular diseases, depression, seasonal affective disorder (SAD), circadian rhythm sleep disorders and sexual dysfunction. Studies by Alfred J. Lewy at Oregon Health & Science University and other researchers have found that it may ameliorate circadian misalignment and SAD. Basic research indicates that melatonin may play a significant role in modulating the effects of drugs of abuse such as cocaine.
Treatment of circadian rhythm disorders
Exogenous melatonin taken in the evening is, together with light therapy upon awakening, the standard treatment for delayed sleep phase syndrome (DSPS) and non-24-hour sleep-wake syndrome. It appears to have some use against other circadian rhythm sleep disorders as well, such as jet lag and the problems of people who work rotating or night shifts. Melatonin reduces sleep onset latency to a greater extent in people with DSPS than in people with insomnia.
Taken 30 to 90 minutes before bedtime, melatonin supplementation acts as a mild hypnotic. It causes melatonin levels in the blood to rise earlier than the brain’s own production accomplishes. This usage is now commonly used in sleep and relaxation drinks.
A very small dose taken several hours before bedtime in accordance with the phase response curve for melatonin in humans (PRC) doesn’t cause sleepiness but, acting as a chronobiotic (affecting aspects of biological time structure), advances the phase slightly and is additive to the effect of using light therapy upon awakening. Light therapy may advance the phase about one to two-and-a-half hours and a small oral dose melatonin, timed correctly some hours before bedtime, can add about 30 minutes to the advance achieved with light therapy.
Research shows that after melatonin is administered to ADHD patients on methylphenidate, the time needed to fall asleep is significantly reduced. Furthermore, the effects of the melatonin after three months showed no change from its effects after one week of use.
Melatonin has been shown to be effective in treating one form of depression, seasonal affective disorder, and is being considered for bipolar and other disorders where circadian disturbances are involved. It has been observed that bipolar disorder might have, as a “trait marker” (something which is characteristic of being bipolar, that does not change with state), supersensitivity to light, i.e. a greater decrease in melatonin secretion in response to light exposure at night. This could be contrasted with drug-free recovered bipolar patients not showing light hypersensitivity.
A systematic review of unblinded clinical trials involving a total of 643 cancer patients using melatonin found a reduced incidence of death. Another clinical trial is due to be completed in 2012. Melatonin levels at night are reduced to 50% by exposure to a low-level incandescent bulb for only 39 minutes, and it has been suspected that women with the brightest bedrooms have an increased risk for breast cancer. Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers.
Yeah, so it’s been working so far 🙂
Tuesday, June 14, 2011, 9:34 pm
So far so good.
Further research into melatonin shows that the recommended dosages are 1mg, and lower dosages are better.
Further research shows that it is very likely I am “D” deficient.
Further research shows that it is very likely I am “C” deficient.
I ran out of “Happy Camper” 2 weeks ago, and the effects were noticeable.
I ran out of “Mood Support” a week ago, and the effects were noticeable.
Health Rider Inversion Table System
Last week I whacked my back again, so my exercise routine has changed a bit, namely I now am doing 10 minutes of stretching on an inversion table, and then 10 side bends (each way) and 10 situps, while inverted, to help strengthen the area.
I’ve also upped my mileage to 5 per day, I’ll probably leave it here for a while.
Today I restocked my “Happy Camper”, “Mood Support” and Melatonin.
I’m changing the Melatonin dosage from 3mg to 1mg, taken nightly at bedtime.
I’m _not_ changing the Happy Camper, Mood support, or Omega 3 dosages at this time.
I also made some other additions to my supplement routine.
Spring Valley Natural C with rose hips 500mg (one per day, in the morning)
You know, to prevent Scurvy 🙂
Spring Valley Maximum Strength D3 5000 iu (one per day, in the morning)
One of the most important roles of vitamin D is to maintain skeletal calcium balance by promoting calcium absorption in the intestines, promoting bone resorption by increasing osteoclast number, maintaining calcium and phosphate levels for bone formation, and allowing proper functioning of parathyroid hormone to maintain serum calcium levels.
Vitamin D deficiency can result in lower bone mineral density and an increased risk of bone loss (osteoporosis) or bone fracture because a lack of vitamin D alters mineral metabolism in the body.
Vitamin D has been studied as a potential treatment for osteoporosis, but since treatment of vitamin D deficiency is associated with an increase of mineralization of osteoid, it remains unclear whether vitamin D has any effect on osteoporotic bone.
In cross-sectional studies there was a positive relationship between vitamin D and bone mineral density in the hip.
Lips (2001) reported that bone mineral deficit in osteomalacia was larger than that in milder degrees of vitamin D deficiency.
There is also a relationship between low bone mineral density and sedentary life style. This is evident in frail, elderly subjects because they are often vitamin D deficient and lead an inactive lifestyle.
Lips (2001) also reported that mild vitamin D deficiency was not associated with an increased risk for hip fracture. A study done in Norway consisted of 246 patients with hip fractures who were studied for risk factors.
Results showed that a vitamin D intake lower than 100 IU/day was associated with an increased risk for hip fracture.
Vitamin D supplements may also increase bone mineral density in other parts of the skeleton.
A study showed that a supplement of 800 IU per day of vitamin D increased the bone mineral density of the lumbar spine in postmenopausal women in comparison with the control group.
Persons over the age of 50 years need higher levels of vitamin D. In a study discussed in LoPiccolo et al. (2010), adults who consumed a daily supplementation with 482–770 IU of vitamin D had reduced fracture rates of 20% for non-vertebral fractures. However, there was no reported reduction in fracture risk for persons who had 400 IU or less of vitamin D daily.
Vitamin D receptor ligands have been shown to increase the activity of natural killer cells, and enhance the phagocytic activity of macrophages.
Active vitamin D hormone also increases the production of cathelicidin, an antimicrobial peptide that is produced in macrophages triggered by bacteria, viruses, and fungi.
Suggestions of a link between vitamin D deficiency and the onset of multiple sclerosis posited that this is due to the immune-response suppression properties of Vitamin D and that vitamin D is required to activate a histocompatibility gene (HLA-DRB1*1501) necessary for differentiating between self and foreign proteins in a subgroup of individuals genetically predisposed to MS.
Whether vitamin D supplements during pregnancy can lessen the likelihood of the child developing MS later in life is not known; however, vitamin D fortification has been suggested to have caused a pandemic of allergic disease and an association between vitamin D supplementation in infancy and an increased risk of atopy and allergic rhinitis later in life has been found. Veteran vitamin D researcher Hector DeLuca has cast doubt on whether vitamin D affects MS.
Tuberculosis and HIV
Historically, vitamin D3 was used to treat tuberculosis patients, but has not been adequately investigated in controlled clinical trials. The hormonally active form of vitamin D3, 1,25-dihydroxycholecalciferol (1,25(OH)2D), has been shown to have antimycobacterial activity in vitro, but the applicability of this effect to clinical situations has not been shown. Vitamin D3 supplementations has not shown any improvement in treating tuberculosis except in a small subset of patients with the tt genotype of the TaqI vitamin D receptor polymorphism. Several studies have shown an association between low serum levels of 25-hydroxycholecalciferol (25(OH)D) and increased risk for both active tuberculosis disease progression and susceptibility. More prospective studies will be required to ascertain the potential role of vitamin D supplementation in treating patients with tuberculosis.
Vitamin D3 has also shown some anti-HIV-1 effects in vitro, including the induction of autophagy. The potential effect in humans has not been investigated. Lower levels of 1,25(OH)2D in HIV infected patients are correlated with significantly lower CD4+ T cell counts and higher tumor necrosis factor levels, which normally decrease in number with progression to AIDS, although no causative association has been shown. In an epidemiological study of HIV positive women in Tanzania, there appeared to be a correlation between reduced levels of Vitamin D and speed of HIV disease progression. These results will need to be confirmed in a blinded clinical trial before dietary recommendations can be made.
See also: Vitamin D and influenza
Lack of vitamin D synthesis is a possible explanation for high rates of influenza infection during winter however, see flu season for the factors apart from vitamin D that are also hypothesized to influence rates of infection during winter. For viral infections, other implicated factors include low relative humidities produced by indoor heating and cold temperatures that favor virus spread during winter.
The molecular basis for thinking that vitamin D has the potential to prevent cancer lies in its role in a wide range of cellular mechanisms central to the development of cancer. These effects may be mediated through vitamin D receptors expressed in cancer cells. Polymorphisms of the vitamin D receptor (VDR) gene have been associated with an increased risk of breast cancer. Women with mutations in the VDR gene had an increased risk of breast cancer.
A 2006 study using data on over 4 million cancer patients from 13 different countries showed a marked increase in some cancer risks in countries with less sun and another metastudy found correlations between vitamin D levels and cancer. The authors suggested that intake of an additional 1,000 international units (IU) (or 25 micrograms) of vitamin D daily reduced an individual’s colon cancer risk by 50%, and breast and ovarian cancer risks by 30%. Low levels of vitamin D in serum have been correlated with breast cancer disease progression and bone metastases. However, the vitamin D levels of a population do not depend on the solar irradiance to which they are exposed. Moreover, there are genetic factors involved with cancer incidence and mortality which are more common in northern latitudes.
A 2006 study found that taking the U.S. RDA of vitamin D (400 IU per day) cut the risk of pancreatic cancer by 43% in a sample of more than 120,000 people from two long-term health surveys. However, in male smokers a 3-fold increased risk for pancreatic cancer in the highest compared to lowest quintile of serum 25-hydroxyvitamin D concentration has been found.
A randomized intervention study involving 1,200 women, published in June 2007, reports that vitamin D supplementation (1,100 international units (IU)/day) resulted in a 60% reduction in cancer incidence, during a four-year clinical trial, rising to a 77% reduction for cancers diagnosed after the first year (and therefore excluding those cancers more likely to have originated prior to the vitamin D intervention). The study was criticized on several grounds including lack of reported data, use of statistical techniques and comparison with a self-selected (i.e. non-randomized) observational study that found long term convergence of breast cancer incidence (i.e. the cancer occurrence had merely been delayed) The author’s response provided the requested data, explained their statistical usage and commented that even if the vitamin D merely delayed the appearance of cancer (which they did not believe, based on other studies), that this was still a considerable benefit.
In 2007, the Canadian Cancer Society recommended that adults living in Canada should consider taking vitamin D supplementation of 1,000 international units (IU) a day during the fall and winter. A US National Cancer Institute study analyzed data from the third national Health and Nutrition Examination Survey to examine the relationship between levels of circulating vitamin D in the blood and cancer mortality in a group of 16,818 participants aged 17 and older. It found no support for an association between 25(OH)D and total cancer mortality. However, the study did find that “colorectal cancer mortality was inversely related to serum 25(OH)D level, with levels 80 nmol/L or higher associated with a 72% risk reduction (95% confidence interval = 32% to 89%) compared with lower than 50 nmol/L, Ptrend = .02.” Unlike other studies, this one was carried out prospectively — meaning that participants were followed looking forward — and the researchers used actual blood tests to measure the amount of vitamin D in blood, rather than trying to infer vitamin D levels from potentially inaccurate predictive models.
A meta-study published in the International Journal of Cancer in May 2010 analyzed 35 independent studies of vitamin D and cancer. The researchers determined that a 10 nanogram/milliliter increase in serum vitamin D is associated with a 15% lower risk of colon cancer. The analysis also found an 11% lower risk for breast cancer, although the authors report that due to case study methodology that this finding is ultimately insignificant.
A 2011 study done at the University of Rochester Medical Center found that low vitamin D levels among women with breast cancer correlate with more aggressive tumors and poorer prognosis. The study associated sub-optimal vitamin D levels with poor scores on every major biological marker that helps physicians predict a patient’s breast cancer outcome. The lead researcher stated, “Based on these results, doctors should strongly consider monitoring vitamin D levels among breast cancer patients and correcting them as needed.”
A report from the National Health and Nutrition Examination Survey (NHANES) involving nearly 5,000 participants found that low levels of vitamin D were associated with an increased risk of peripheral artery disease (PAD). The incidence of PAD was 80% higher in participants with the lowest vitamin D levels (<17.8 ng/mL). Cholesterol levels were found to be reduced in gardeners in the UK during the summer months. Low levels of vitamin D are associated with an increase in high blood pressure and cardiovascular risk. Numerous observational studies show this link, but of two systemic reviews one found only weak evidence of benefit from supplements and the other found no evidence of a beneficial effect whatsoever.
There is a certain amount of evidence to suggest that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages. These findings raise questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk. Calcifediol (25-hydroxy-vitamin D) is implicated in the etiology of atherosclerosis, especially in non-Caucasians. Freedman et al. (2010) found that serum vitamin D correlates with calcified atheroscleratic plaque (CP) in African Americans, but not in Euro-Americans, “Higher levels of 25-hydroxyvitamin D seem to be positively associated with aorta and carotid CP in African Americans but not with coronary CP. These results contradict what is observed in individuals of European descent.” One study found an elevated risk of ischaemic heart disease in Southern India in individuals whose vitamin D levels were above 89 ng/mL. A review of vitamin D status in India concluded that studies uniformly point to low 25(OH)D levels in Indians despite abundant sunshine, and suggested a public health need to fortify Indian foods with vitamin D might exist. The levels found in India are consistent with many other studies of tropical populations which have found that even an extreme amount of sun exposure, such as incurred by rural Indians, does not raise 25(OH)D levels to the levels typically found in Europeans.
Using information from the National Health and Nutrition Examination Survey a large scale study concluded that having low levels of vitamin D (<17.8 ng/ml) was independently associated with an increase in all-cause mortality in the general population. However it has been pointed out that increased mortality was also found in those with higher concentrations, (above 50 ng/ml). A sophisticated August 2010 study of plasma vitamin D and mortality in older men concluded that both high (>39 ng/ml) and low (<18 ng/ml)) concentrations of plasma 25(OH)D are associated with elevated risks of overall and cancer mortality compared with intermediate concentrations. These boundaries were less than suggested by the Melamed et al. study of National Health and Nutrition Examination Survey data but the immunoassay used by National Health and Nutrition Examination Survey tended to overestimate vitamin D values.
Overall, excess or deficiency in the calciferol system appear to cause abnormal functioning and premature aging.
Complex regulatory mechanisms control metabolism and recent epidemiological evidence suggests that there is a narrow range of vitamin D blood levels in which metabolic functions are optimized. Levels above or below this natural homeostasis of vitamin D are associated with increased mortality.
NOW 5-HTP “neurotransmitter support” 50mg (one per day, in the evening)
Note that this is taking the 20mg of 5-HTP in “Mood Support” up to 70mg.
5-HTP has been studied and shown to be of benefit in the following conditions: depression, anxiety, binge eating associated with obesity, and insomnia.
Based on the occurrence of serious side effects and drug interactions (q.v.), particularly in long-term use in form of dietary supplements that are often not communicated to the treating physician, its use is no longer recommended. In addition, due to unspecific effects, the risk/benefit ratio compared to serotonin reuptake inhibitors and other serotonergic antidepressant drugs is not favorable for 5-HTP containing supplements.
I’m going to walk softly with this, and if i don’t see any changes in a week I will probably stop taking it, as things like:
“Direct and indirect evidence for possible yet unproven risks and side effects associated with 5-HTP when overdosed: Heart valve damage or disease (cardiac fibrosis). When combined with MAOIs or SSRIs, 5-HTP can cause acute serotonin syndrome.”
Are warnings I do not take lightly.
I feel comfortable with this at this time, as it is widely agreed upon that excess 5-HTP, especially when administered with Vitamin B6, is thought to be metabolized and excreted, and I’m taking *a lot* of B6.
I’m also looking into:
NOW L-Tryptophan 500mg (one per day, before bedtime)
For many organisms (including humans), tryptophan is an essential amino acid. This means that it cannot be synthesized by the organism and therefore must be part of its diet. Amino acids, including tryptophan, act as building blocks in protein biosynthesis. In addition, tryptophan functions as a biochemical precursor for the following compounds (see also figure to the right):
Serotonin (a neurotransmitter), synthesized via tryptophan hydroxylase. Serotonin, in turn, can be converted to melatonin (a neurohormone), via N-acetyltransferase and 5-hydroxyindole-O-methyltransferase activities.
Niacin is synthesized from tryptophan via kynurenine and quinolinic acids as key biosynthetic intermediates.
Auxin (a phytohormone) when sieve tube elements undergo apoptosis tryptophan is converted to auxins.
The disorders fructose malabsorption and lactose intolerance cause improper absorption of tryptophan in the intestine, reduced levels of tryptophan in the blood and depression.
In bacteria that synthesize tryptophan, high cellular levels of this amino acid activate a repressor protein, which binds to the trp operon. Binding of this repressor to the tryptophan operon prevents transcription of downstream DNA that codes for the enzymes involved in the biosynthesis of tryptophan. So high levels of tryptophan prevent tryptophan synthesis through a negative feedback loop and, when the cell’s tryptophan levels are reduced, transcription from the trp operon resumes. The genetic organisation of the trp operon thus permits tightly regulated and rapid responses to changes in the cell’s internal and external tryptophan levels.
Tryptophan is a routine constituent of most protein-based foods or dietary proteins. It is particularly plentiful in chocolate, oats, dried dates, milk, yogurt, cottage cheese, red meat, eggs, fish, poultry, sesame, chickpeas, sunflower seeds, pumpkin seeds, spirulina, and peanuts. Despite popular belief that turkey has a particularly high amount of tryptophan, the amount of tryptophan in turkey is typical of most poultry.
Since other than cheese, and the occasional ice cream, I avoid all dairy, and I have avoided all nuts for years, (although one would think that my intake of red meat, eggs, fish, and poultry would be enough).
To take this one, It looks like I may have to drop the Mood Support, due to the potential for serotonin overdose when combined with St Johns Wort.
so far, so good 🙂