Q. I've had mild depression for a long long long time...(maybe 10 years). I'm just wondering if perhaps certain deficiencies lead to depression and if there is a way I can be tested for deficiencies. For example, I know a lack of vitamin B can have effect on mood. How do they test vitamin b levels?
And what about hormonal imbalances? Can that lead to depression as well?
And what about hormonal imbalances? Can that lead to depression as well?
A. Deficiencies in the following vitamins and minerals can lead to chemical imbalances in the brain that can cause symptoms of depression -
- B Vitamins (e.g. B1, B6, B12, B9)
- Vitamin D
- Selenium
Clinical research shows that a diet and lifestyle contributing to low levels of these vitamins and minerals may contribute to feelings of depression, anxiety and fatigue. Unfortunately, many adults do not receive the optimal amount of these vital nutrients.
Hormonal imbalances can also lead to signs and symptoms of depression as well. According to allaboutdepression.com, "The hypothalamus also controls the function of the pituitary gland which in turn regulates key hormones. Other structures within the limbic system that are associated with emotional reaction are the amygdala and hippocampus. The activities of the limbic are so important and complex that disturbances in any part of it, including how neurotransmitters function, could affect your mood and behavior."
- B Vitamins (e.g. B1, B6, B12, B9)
- Vitamin D
- Selenium
Clinical research shows that a diet and lifestyle contributing to low levels of these vitamins and minerals may contribute to feelings of depression, anxiety and fatigue. Unfortunately, many adults do not receive the optimal amount of these vital nutrients.
Hormonal imbalances can also lead to signs and symptoms of depression as well. According to allaboutdepression.com, "The hypothalamus also controls the function of the pituitary gland which in turn regulates key hormones. Other structures within the limbic system that are associated with emotional reaction are the amygdala and hippocampus. The activities of the limbic are so important and complex that disturbances in any part of it, including how neurotransmitters function, could affect your mood and behavior."
Which of the following explains why B vitamin deficiencies lead to lack of energy?
Q. a.)B vitamins are a source of kilocalories
b.) Absorption of carbohydrates and fats is decreased
c.) Oxygen for energy metabolism cannot be transported to the cells
d.) Coenzymes needed for energy metabolism are produced in insufficient amounts
Is it D? Since symptoms of Vitamin B deficiences directly reflect the disturbances of metabolism incurred by a coenzumes
b.) Absorption of carbohydrates and fats is decreased
c.) Oxygen for energy metabolism cannot be transported to the cells
d.) Coenzymes needed for energy metabolism are produced in insufficient amounts
Is it D? Since symptoms of Vitamin B deficiences directly reflect the disturbances of metabolism incurred by a coenzumes
A. Answer d)
Exaplanation:
Vitamin B group vitamins are required as coenzymes for the cytochrome system (electron chain) stage of aerobic respiration when most of the ATP is produced.
Exaplanation:
Vitamin B group vitamins are required as coenzymes for the cytochrome system (electron chain) stage of aerobic respiration when most of the ATP is produced.
How long does it take Vitamin B-12 to be absorbed into my system?
Q. After research as to my lack of energy lately, I came across a few people who suggested taking Vitamin B-12 as it is responsible for energy metabolisim and I may be deficient. After reading some blogs and the packaging on the actual vitamins I decided to go with the sublingul (under the tongue) form as it is abosrbed into my system faster. I am taking the reccommended dosage once a day and It is working beautifuly although I'm wondering if I am feeling energy when I do because the Vitamin kicks in or if it's a placibo effect. Does anybody know how long it takes to be absorbed...minutes...hours...your response is much appreciated.
A. Physiology of Absorption, Metabolism, and Excretion
Following ingestion, absorption of thiamin occurs mainly in the jejunum, at lower concentrations as an active, carrier-mediated system involving phosphorylation and at higher concentrations by passive diffusion. Thiamin is transported in blood both in erythrocytes and plasma.
Only a small percentage of a high dose of thiamin is absorbed, and elevated serum values result in active urinary excretion of the vitamin (Davis et al., 1984). After an oral dose of thiamin, peak excretion occurs in about 2 hours, and excretion is nearly complete after 4 hours (Levy and Hewitt, 1971; Morrison and Campbell, 1960). In a study by Davis and colleagues (1984), a 10-mg oral dose of thiamin was given in water, and the mean serum thiamin peaked at 24 nmol/L (7.2 µg/L) �42 percent above baseline. Within 6 hours the serum thiamin concentration had returned to baseline, 17 nmol/L (5.2 µg/L). Prompt urinary excretion of thiamin was also reported by Najjar and Holt (1940) and McAlpine and Hills (1941).
With higher pharmacological levels, namely repetitive 250-mg amounts taken orally and 500 mg given intramuscularly, nearly 1 week was required for steady state plasma concentrations to be reached; a mean elimination half-life of 1.8 days was estimated (Royer-Morrot et al., 1992).
Total thiamin content of the adult human has been estimated to be approximately 30 mg, and the biological half-life of the vitamin is probably in the range of 9 to 18 days (Ariaey-Nejad et al., 1970).
Clinical Effects of Inadequate Intake
Early stages of thiamin deficiency may be accompanied by non-specific symptoms that may be overlooked or easily misinterpreted (Lonsdale and Shamberger, 1980). The clinical signs of deficiency include anorexia; weight loss; mental changes such as apathy, decrease in short-term memory, confusion, and irritability; muscle weakness; and cardiovascular effects such as an enlarged heart (Horwitt et al., 1948; Inouye and Katsura, 1965; Platt, 1967; Williams et al., 1942; Wilson, 1983). In wet beriberi, edema occurs; in dry
Following ingestion, absorption of thiamin occurs mainly in the jejunum, at lower concentrations as an active, carrier-mediated system involving phosphorylation and at higher concentrations by passive diffusion. Thiamin is transported in blood both in erythrocytes and plasma.
Only a small percentage of a high dose of thiamin is absorbed, and elevated serum values result in active urinary excretion of the vitamin (Davis et al., 1984). After an oral dose of thiamin, peak excretion occurs in about 2 hours, and excretion is nearly complete after 4 hours (Levy and Hewitt, 1971; Morrison and Campbell, 1960). In a study by Davis and colleagues (1984), a 10-mg oral dose of thiamin was given in water, and the mean serum thiamin peaked at 24 nmol/L (7.2 µg/L) �42 percent above baseline. Within 6 hours the serum thiamin concentration had returned to baseline, 17 nmol/L (5.2 µg/L). Prompt urinary excretion of thiamin was also reported by Najjar and Holt (1940) and McAlpine and Hills (1941).
With higher pharmacological levels, namely repetitive 250-mg amounts taken orally and 500 mg given intramuscularly, nearly 1 week was required for steady state plasma concentrations to be reached; a mean elimination half-life of 1.8 days was estimated (Royer-Morrot et al., 1992).
Total thiamin content of the adult human has been estimated to be approximately 30 mg, and the biological half-life of the vitamin is probably in the range of 9 to 18 days (Ariaey-Nejad et al., 1970).
Clinical Effects of Inadequate Intake
Early stages of thiamin deficiency may be accompanied by non-specific symptoms that may be overlooked or easily misinterpreted (Lonsdale and Shamberger, 1980). The clinical signs of deficiency include anorexia; weight loss; mental changes such as apathy, decrease in short-term memory, confusion, and irritability; muscle weakness; and cardiovascular effects such as an enlarged heart (Horwitt et al., 1948; Inouye and Katsura, 1965; Platt, 1967; Williams et al., 1942; Wilson, 1983). In wet beriberi, edema occurs; in dry
Vitamin B 12 deficiency and post Lyme disease?
Q. I went on antibiotics and now I'm off of them. I have still been having headaches and fatigue, sometimes its hard to concentrate. I did a blood test and there is no sign of active Lyme in my system. So i did not know what was wrong. I been taking vitamin b 12 supplement and noticed these symptoms are getting better.
Is there a link between B 12 deficiency and the Lyme bacteria?
Is there a link between B 12 deficiency and the Lyme bacteria?
A. Several common features of modern life accelerate the decline of vitamin B12 in serum through life, including the following:
* Microwave ovens In one test, microwaving milk degenerated 30% to 40% of milk's vitamin B12 in six minutes; with conventional heating, 25 minutes of boiling was needed to depress B12 that much. (67) More importantly, the heat of microwaving destroys all the enzymes in ingested food, which are required to enable absorption and utilization of food. And so by eating microwaved food, both at home and in restaurant and take-out meals, tens of millions of Americans are making themselves increasingly vulnerable to AD, as well as to cancer.
* The Western diet B12 ingestion and stores tend to be insufficient among millions who have for decades eaten RDA-fortified, yet vitamin- and mineral-depleted, processed Western diets, which are also big sources of disease-creating free radicals. (69) Too low levels of omega-3 essential fatty acids in Western diets, harmful in many ways, must also contribute to insufficient B12 levels. (70) Omega-3 supplementation may yield its benefits largely through augmenting vitamin B12. Too-low levels of acetyl-carnitine and folic acid also appear to worsen risk of the condition. (71,72) It's worth noting that in an Alzheimer's disease mouse model, a diet rich in omega-3 essential fatty acids, specifically DHA (docosahexaenoic acid), has been shown to potentially slow or even prevent Alzheimer's disease. (73) At modest cost, we can easily ingest DHA in fish oil or [Carlson's] cod liver oil. Also worth considering is the role of trans-fatty acids (TFA) found in products labeled "zero trans-fats" with EPA approval. In a study of over 800 senior citizens, those with high TFA were twice as likely to suffer symptoms of Alzheimer's disease compared to those with the lowest TFA intake (hsiresearch@healthiernews.com; accessed 2/17/06).
*Hypochlorhydria.i.e. insufficient hydrochloric acid Most commonly, B12 insufficiency results directly from hypochlorhydria--insufficient hydrochloric acid (HCl) in the stomach--or by achlorhydria--no HCI at all. The acid should be concentrated enough to dissolve a nail in an hour. (77) Hypochlorhydria is likely caused by zinc/vitamin B6 deficiency (78) and a shortage of ionized calcium. (79,80) (Both deficiencies are typically present in older people.) Lack of enough pepsin or HCl in the stomach to generate the bond between B12 and its carrier protein typically shows with atrophic gastritis. (81,82) Both are also risk factors for gastric cancer. (83) Incomplete digestion of foods due to hypochlorhydria and low pepsin production also can be involved in subsequent allergic response in asthma.
* Microwave ovens In one test, microwaving milk degenerated 30% to 40% of milk's vitamin B12 in six minutes; with conventional heating, 25 minutes of boiling was needed to depress B12 that much. (67) More importantly, the heat of microwaving destroys all the enzymes in ingested food, which are required to enable absorption and utilization of food. And so by eating microwaved food, both at home and in restaurant and take-out meals, tens of millions of Americans are making themselves increasingly vulnerable to AD, as well as to cancer.
* The Western diet B12 ingestion and stores tend to be insufficient among millions who have for decades eaten RDA-fortified, yet vitamin- and mineral-depleted, processed Western diets, which are also big sources of disease-creating free radicals. (69) Too low levels of omega-3 essential fatty acids in Western diets, harmful in many ways, must also contribute to insufficient B12 levels. (70) Omega-3 supplementation may yield its benefits largely through augmenting vitamin B12. Too-low levels of acetyl-carnitine and folic acid also appear to worsen risk of the condition. (71,72) It's worth noting that in an Alzheimer's disease mouse model, a diet rich in omega-3 essential fatty acids, specifically DHA (docosahexaenoic acid), has been shown to potentially slow or even prevent Alzheimer's disease. (73) At modest cost, we can easily ingest DHA in fish oil or [Carlson's] cod liver oil. Also worth considering is the role of trans-fatty acids (TFA) found in products labeled "zero trans-fats" with EPA approval. In a study of over 800 senior citizens, those with high TFA were twice as likely to suffer symptoms of Alzheimer's disease compared to those with the lowest TFA intake (hsiresearch@healthiernews.com; accessed 2/17/06).
*Hypochlorhydria.i.e. insufficient hydrochloric acid Most commonly, B12 insufficiency results directly from hypochlorhydria--insufficient hydrochloric acid (HCl) in the stomach--or by achlorhydria--no HCI at all. The acid should be concentrated enough to dissolve a nail in an hour. (77) Hypochlorhydria is likely caused by zinc/vitamin B6 deficiency (78) and a shortage of ionized calcium. (79,80) (Both deficiencies are typically present in older people.) Lack of enough pepsin or HCl in the stomach to generate the bond between B12 and its carrier protein typically shows with atrophic gastritis. (81,82) Both are also risk factors for gastric cancer. (83) Incomplete digestion of foods due to hypochlorhydria and low pepsin production also can be involved in subsequent allergic response in asthma.
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