Essential fatty acids and B vitamin supplements helps those with Schizophrenia

Discussion in 'Food and nutrition' started by Roman Bystrianyk, Jan 17, 2006.

  1. http://www.healthsentinel.com/org_news.php?event=org_news_print_list_item&id=074

    Roman Bystrianyk, "Essential fatty acids and B vitamin supplements
    helps those with Schizophrenia", Health Sentinel, January 18, 2006,

    According to the Website Schizophrenia.com, schizophrenia is a chronic,
    severe, and disabling brain disease. Approximately 1 percent of the
    population develops schizophrenia during their lifetime, with more than
    2 million Americans suffering from the illness in a given year. Life
    expectancy of patients with schizophrenia is 20% shorter than normal.

    Studies have shown that patients with schizophrenia have low levels of
    essential fatty acids. The omega-6 fatty acid, arachidonic acid or AA,
    the omega-3 fatty acid, docosahexaenoic acid or DHA, have shown the
    most consistent association. Low dietary intake of DHA and AA are
    associated with an increase of psychiatric symptoms. Six out of seven
    studies that have examined EPA supplementation found positive results
    in psychiatric symptoms.

    Patients with schizophrenia have also been found to have low levels of
    B vitamins. Low B vitamins can be noticed when there is an elevated
    homocysteine. Homocysteine is a toxic waste product produced during
    cellular metabolism. A high level of homocysteine is a risk factor for
    coronary artery disease. Elevated homocysteine is likely involved in
    degenerative disorders like Alzheimer's, and psychiatric disorders
    such as schizophrenia.

    In the journal Prostaglandins, Leukotrienes and Essential Fatty Acids,
    study authors examined the effects of fatty acid and B vitamin
    supplements over 12 weeks on 4 patients diagnosed with schizophrenia. 5
    of 61 patients had moderate hyperhomocysteinemia (30-100 micromol/L)
    and 2/61 patients had essential fatty acid deficiency (mead acid,
    20:3n-9>0.46 mol%). These findings are rare in healthy adults and point
    to severe deficiencies or metabolic disorders. The fatty acid
    supplement was composed of approximately 310 mg EPA, 200 mg DHA, 1 gram
    ALA (alpha-linolenic acid), and 7 grams LA (linoleic acid). The B
    vitamin supplement was composed of 800 micrograms folic acid, 8 mg B6,
    and 4 micrograms B12.

    The study authors found that as a group, schizophrenics had low omega-6
    and omega-3 fatty acids and increased homocysteine. These conditions
    "proved easily correctable by supplementation." There is compelling
    evidence that supplementation with B-vitamins to reduce homocysteine
    and supplementation with omega-3 fatty acids decrease the risk of heart
    disease.

    Newer antipsychotic drugs may have side effects such as weight gain,
    elevated trigylcerides, and increased risk of diabetes. All of these
    "constitute a risk of cardiovascular disease in a population segment
    with little exercise, poor diet, almost universal smoking, and
    unhealthy lifestyle in general. In other words, patients with
    psychiatric disease, especially patients with schizophrenia, may
    benefit from good nutrition." Importantly, none of the patients with
    essential fatty acid deficiency, increased homocysteine, or both were
    suspected by their doctors to have a poor diet.

    Lead author of the study, Ramses F.J. Kemperman, M.Sc., noted that,
    "Unfortunately we did not measure psychopathology on the PANSS or any
    other psychiatric symptom rating scale." The Positive and Negative
    Syndrome Scale (PANSS) is a 30-item scale with 16 general
    psychopathology symptom items, seven positive-symptom items, and seven
    negative symptom items. Dr. Kemperman continued, "However, 75% of
    patients self-reported a general improvement in well-being, although
    this could not be confirmed by observations of their treating
    psychiatrist."

    SOURCE: Prostaglandins, Leukotrienes and Essential Fatty Acids, 2005
    Dec 26; [Epub ahead of print]
     
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  2. Jim Chinnis

    Jim Chinnis Guest

    "Roman Bystrianyk" <[email protected]> wrote in part:

    >There is compelling
    >evidence that supplementation with B-vitamins to reduce homocysteine
    >... decrease the risk of heart
    >disease.


    I believe the evidence, taken as a whole, actually shows that
    supplementation with B-vitamins to reduce homocysteine has no effect on the
    risk of heart disease.
    --
    Jim Chinnis Warrenton, Virginia, USA [email protected]
     
  3. For your consideartion:

    Roman Bystrianyk, "Homocysteine and Heart Disease - A Look at Vitamin
    B12", Health Sentinel, July 15, 2005,

    An elevated blood homocysteine level is a strong risk factor for heart
    disease and stroke. Homocysteine is a toxic waste product produced
    during metabolism of an amino acid called methionine. Diets high in
    meat and dairy generate excess methionine, which is converted by the
    body into homocysteine.

    Folic acid and other B vitamins help break down homocysteine in the
    body. Studies have shown that higher blood levels of B vitamins are
    related to lower concentrations of homocysteine, and additional
    evidence demonstrates that low blood levels of folic acid are linked
    with an increased risk of fatal heart attack and stroke.

    Folic acid fortification of cereal products began in North America in
    1996 and was made mandatory in 1998. Studies have shown that
    fortification has reduced the number of neural tube defects by 50%
    however, little impact has been observed in death from heart disease.
    Now that folic acid fortification is widespread, vitamin B12 has become
    the next important factor in homocysteine levels.

    The June 2005 issue of the Canadian Medical Association Journal
    examines how many people are low in vitamin B12 and the relationship of
    vitamin B12 to homocysteine and plaque buildup in the carotid artery.
    The study authors examined 421 people with an average of 66 years,
    checking their vitamin B12 levels; homocysteine levels; and build up of
    plaque in their carotid artery.

    They found that nearly 1 in 5 of the group had a vitamin B12
    deficiency. The authors note that this value may be an
    "underestimate" as only 10% of the patient group had the specific
    test measuring for deficiency. The authors also found that,
    "homocysteine levels fell significantly as vitamin B12 levels rose
    and that plaque in the carotid artery "increased markedly above
    levels of homocysteine that would usually be regarded as low (7.7
    µmol/L)."

    Although the recommended daily intake of vitamin B12 is 6 micrograms,
    one study showed that among elderly patients "1000 micrograms daily
    is required for adequate absorption."

    The investigators also found that creatinine levels to be "a strong a
    predictor of homocysteine level as were vitamin B12 levels."
    Creatinine is the waste product of creatine catabolism and is a
    by-product of muscle activity normally removed from the blood by the
    kidneys. The relationship between vitamin B12 and creatinine was strong
    enough to be "worthy of further investigation."

    In conclusion, the authors found that, "vitamin B12 deficiency is
    surprisingly common among patients with vascular disease." The
    "striking" inverse relationship between vitamin B12 and
    homocysteine "suggests a key role for vitamin B12 in the treatment of
    elevated homocysteine levels for vascular disease."

    SOURCE: Canadian Medical Association Journal, June 2005
     
  4. Jim Chinnis

    Jim Chinnis Guest

    Yes, there are lots of associations. What I am saying is that no one has
    shown that supplementing with B vitamins (and thereby reducing homocysteine)
    actually reduces the risk of developing heart disease or of having heart
    attacks. What data there are seem to contradict that idea.
    --
    Jim Chinnis Warrenton, Virginia, USA [email protected]
     
  5. I understand your point. Thank you for clarifying. Here is a single
    study that I have that may be of interest.

    Long-term improvement in homocysteine levels and arterial endothelial
    function after 1-year folic acid supplementation

    Kam S. Woo, MD; Ping Chook, MD; Lindy L. T. Chan; Alice S. P. Cheung;
    Wing H. Fung, MChB; Mu Qiao, MBBS; Yvette I. Lolin, PhD; G. N. Thomas,
    PhD; John E. Sanderson, MD; Con Metreweli, MD; and David S. Celermajer,
    PhD, "Long-term improvement in homocysteine levels and arterial
    endothelial function after 1-year folic acid supplementation", American
    Journal of Medicine, May 1, 2002, Vol. 112, Num. 0, pp. 535-539

    "PURPOSE: Hyperhomocysteinemia, a risk factor for atherosclerosis, is
    associated with endothelial dysfunction that can be improved with
    short-term folic acid supplementation. The current study aimed to
    assess whether folic acid supplementation could produce longer-term
    improvements in homocysteine levels and arterial endothelial function.
    SUBJECTS AND METHODS: Twenty-nine healthy adults with
    hyperhomocysteinemia were selected from 89 volunteers enrolled in a
    community-based atherosclerosis screening project. All subjects were
    given folic acid (10 mg/d) for 1 year. Fasting plasma homocysteine
    levels were measured by high-performance liquid chromatography.
    Arterial endothelial function was measured as flow-mediated dilation of
    the brachial artery using high-resolution B-mode ultrasound. RESULTS:
    Folic acid supplementation for 1 year was associated with a significant
    increase in mean (+/-SD) plasma folate levels (24 +/- 5 nmol/L to 40
    +/- 5 nmol/L; P < 0.001) and a significant decline in homocysteine
    levels (9.0 +/- 1.7 micromol/L to 7.9 +/- 2.0 micromol/L; P < 0.001).
    Flow-mediated dilation also improved significantly, from 7.4% +/- 2.0%
    to 8.9% +/- 1.5% (P <0.0001), but there was no change in
    nitroglycerin-induced (endothelium-independent) responses. CONCLUSIONS:
    These results demonstrate that long-term folic acid improves arterial
    endothelial function and has potential implications for the prevention
    of atherosclerosis in adults with hyperhomocysteinemia."

    "Elevated homocysteine levels are associated with coronary artery,
    cerebrovascular, and peripheral vascular disease. Moderate
    hyperhomocysteinemia is an independent risk factor for atherosclerosis,
    and impaired arterial endothelial function is detectable in healthy
    adults with hyperhomocysteinemia. Homocysteine-related damage to
    intimal cells has been attributed to oxidative stress, production of
    hydrogen peroxide and superoxide, inactivation of nitric oxide, and
    inhibition of glutathione peroxidase activity and synthesis."

    "Folate derivatives lower homocysteine levels by increasing the rate of
    recycling of homocysteine to methionine. In asymptomatic adults with
    hyperhomocysteinemia, folic acid supplementation for 8 weeks improves
    arterial endothelial function. Whether the beneficial effects of folic
    acid on homocysteine levels and arterial endothelial function persist
    over longer periods is not known."

    "All 29 subjects completed the 1-year period with folic acid
    supplementation. No adverse events were encountered, and tablet counts
    revealed > 90% compliance with all study medications in all
    participants."

    "Two subjects (7%) had no substantial changes in homocysteine levels
    despite an increase in their folate levels. There were no significant
    change in body mass index or in creatinine, cholesterol, of vitamin
    B12."

    "In this long-term (1 year) study, folic acid supplementation reduced
    homocysteine levels (by 12%) and increased folic acid levels (by 69%),
    improving endothelial function in asymptomatic subjects. Both total and
    LDL cholesterol levels were within normal ranges at baseline, and there
    were no significant changes 1 year later."

    "In cross-sectional studies, a fasting total homocysteine level > 14
    µmol/L has been associated with atherosclerosis, and it has been
    suggest that a homocysteine level of 10 µmol/L should be the target
    upper limit of normal. In our study, the mean fasting homocysteine
    level was 9 µmol/L, well below the "desirable" upper limit. Thus,
    we observed an improvement in endothelial function after folic acid
    supplementation (10 mg/d) in healthy subjects with relatively normal
    homocysteine levels. However, there is no consensus on the optimal dose
    of folic acid for lowering homocysteine levels. Other vitamins, such as
    B6 and B12, can also be used to lower homocysteine levels, but their
    effects on endothelial function are not known. Other studies have found
    that 2 to 3 months of supplementation with folic acid (5 mg/d) and
    vitamins (C, E, or B12) improved endothelial function of patients with
    coronary artery disease. However, the safety of long-term high-dose
    folic acid supplementation, which might precipitate neurologic
    dysfunction in patients with vitamin B12 deficiency, has not been
    studied."

    "Endothelial dysfunction is a marker of subclinical atherosclerosis and
    is associated with an increased risk of cardiovascular events."

    "This study had several limitations. It was not randomized or placebo
    controlled, and the sample size was small. We used a relatively high
    dose (10 mg/d) of folate; it is possible that lower doses might be
    sufficient. However, a recent study reported that optimization of
    dietary folate or low-dose (400 µg/d) folic acid supplementation
    lowered homocysteine levels but did not enhance endothelial function in
    healthy adults."

    "In conclusion, we found that 1 year of folic acid supplementation
    decreases plasma homocysteine levels and improves arterial endothelial
    function in asymptomatic adults who have homocysteine levels in the
    high-normal range and normal cholesterol levels. Our results support
    the possibility of a long-term beneficial effect of folic acid
    supplementation on the atherosclerotic process."
     
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