Niacin and coenzyme q10

[hardasnails1973]

If a person has low cholesterol of 126 and low hdl as well as takes niacin 1000 mgs to help increase the HDL. Could the niacin be acting like a statin drug and lowering the person coenyzme q10 since they already have low cholesterol to begin with? Would niacin act asHMG Co-A reductase inhibitors?

Found this in google.
it is postulated that high doses of niacin may cause hepatic impairment, which could lead to decreased hepatic extraction of HMG-CoA reductase inhibitors.

[DrMariano2]

@hardasnails1973 731 wrote:

If a person has low cholesterol of 126 and low hdl as well as takes niacin 1000 mgs to help increase the HDL. Could the niacin be acting like a statin drug and lowering the person coenyzme q10 since they already have low cholesterol to begin with? Would niacin act asHMG Co-A reductase inhibitors?

Found this in google.
it is postulated that high doses of niacin may cause hepatic impairment, which could lead to decreased hepatic extraction of HMG-CoA reductase inhibitors.

Niacin does not act as an HMG-CoA reductase inhibitor.

Here is a comparison:

http://cme.medscape.com/viewarticle/540421_print

LDL-C is a better indicator of cardiac risk. It should be < 100.

A cholesterol < 140 would impair steroid hormone production. Why lower it further?

[hardasnails1973]

My hdl are less then 40 despite exercise , proper nutritoin, they have not came up at all that is why I am on 1000 mgs of niacin. My lp (a) is also elevated as well which niacin and vitamin C, lysine helps lower.

I also read that low lysine in relationship to argine may also result in hypocholestemia.
Manganese deficiency which could also be possible factor as my hair analysis is low

I agree with you 100% about low cholesterol, but genetically it has been low all my life. My lowest reading was at age of 15 with total cholesterol of 90 and I was eating about 6,000 caloires a day because I was practicing diving 6 hours 4-5 days a week.

No matter how much red meat, whole organic eggs,butter, EVCO I consume it will not raise cholesterol.

One reason may be that I do eat a low-moderate carbohydrate, no sugar (1 piece of fruit a day), low to no grain diet, with high sat fats (all good sources).

Couldn’t low cholesterol be an indicator of insulin deficiency as well since people with insulin resistance have high cholesterol

Have you seen some one have insulin resistance with low cholesterol, good LDL, low triglycerides

Is there such a condition of super insulin sensitivity?
Too many carbs makes me tired and fatgued similar.

After 2 hours after my meal my blood sugar is back to 85 which I though was good.

About 3 years ago I took in 6 mgs of copper for 3 week, with 3 TBSP of EVCO a day then did a blood test and my blood level of HDL shut up to 69. Maybe this was an indication of potential copper deficiency that long ago, but I never was able to make the connection.

The ND had me on zinc 80 mgs a day for 6 months but he forgot to tell me to take copper.

I recalibrated by supplements to help raise ferritin levels
30 mgs of zinc
2 mgs of copper
100 mgs of iron
30 mgs of mangese

My recent hair analysis should a super high zinc:cu ratio (16) normal is 8
Looking at excessive zinc side effects would be low HDL, but no alterations in CBC to indicate copper anemia.

[DrMariano2]

@hardasnails1973 753 wrote:

My hdl are less then 40 despite exercise , proper nutritoin, they have not came up at all that is why I am on 1000 mgs of niacin. My lp (a) is also elevated as well which niacin and vitamin C, lysine helps lower.

I also read that low lysine in relationship to argine may also result in hypocholestemia.
Manganese deficiency which could also be possible factor as my hair analysis is low

I agree with you 100% about low cholesterol, but genetically it has been low all my life. My lowest reading was at age of 15 with total cholesterol of 90 and I was eating about 6,000 caloires a day because I was practicing diving 6 hours 4-5 days a week.

No matter how much red meat, whole organic eggs,butter, EVCO I consume it will not raise cholesterol.

One reason may be that I do eat a low-moderate carbohydrate, no sugar (1 piece of fruit a day), low to no grain diet, with high sat fats (all good sources).

Couldn’t low cholesterol be an indicator of insulin deficiency as well since people with insulin resistance have high cholesterol

Have you seen some one have insulin resistance with low cholesterol, good LDL, low triglycerides

Is there such a condition of super insulin sensitivity?
Too many carbs makes me tired and fatgued similar.

After 2 hours after my meal my blood sugar is back to 85 which I though was good.

About 3 years ago I took in 6 mgs of copper for 3 week, with 3 TBSP of EVCO a day then did a blood test and my blood level of HDL shut up to 69. Maybe this was an indication of potential copper deficiency that long ago, but I never was able to make the connection.

The ND had me on zinc 80 mgs a day for 6 months but he forgot to tell me to take copper.

I recalibrated by supplements to help raise ferritin levels
30 mgs of zinc
2 mgs of copper
100 mgs of iron
30 mgs of mangese

My recent hair analysis should a super high zinc:cu ratio (16) normal is 8
Looking at excessive zinc side effects would be low HDL, but no alterations in CBC to indicate copper anemia.

If cholesterol already is < 140 and LDL-cholesterol is already good, adjusting HDL cholesterol with Niacin may not be useful, and may instead cause side effect such as impaired concentration and memory. Cholesterol is an important component of cellular membranes. It makes up HALF of the dry weight of the brain. Lowering cholesterol production may instead worsen cellular metabolism and intercellular signaling.

The most important target for reducing the risk of a heart attack is not cholesterol. It is inflammation. Without inflammation, high cholesterol does not lead to atherosclerotic plaque formation. When cholesterol is already low, targeting inflammation is far more useful than attempting to increase HDL-cholesterol. Reducing inflammation – such as by targeting excessive pro-inflammatory signaling – also helps reduce mood problems, cognitive problems, HPA Axis dysregulation, aches and pain, inflammatory diseases, etc.

Cholesterol is synthesized from blood from sugars. Those who eat high animal protein, high saturated fat, high cholesterol meals actually have lower cholesterol than those who eat higher carb meals.

A severely low carbohydrate diet can cause functional problems – unless one is on an Eskimo or Masai style total animal source diet. Carbs are necessary to help prevent the body from targetting proteins and amino acids as an energy source, for example. This may lead to amino acid deficiencies, and other imbalances, etc.

When HPA Axis dysregulation is present, then carbohydrate intake can make a person fatigued. Excessive carbohydrate intake can shut down adrenal function, resulting in lower cortisol levels, which lowers gluconeogenesis. Once glucose normalizes after a carb meal, impaired gluconeogenesis results in low blood sugars (which to me is < 93). Adrenal support treatment using cortisol and DHEA alone is frequently a bandage treatment and won't reset HPA Axis regulation. The actual contributing factors – immune system overactivity, excessive pro-inflammatory cytokine signaling, stress, nutritional deficiencies, thyroid problems, etc. etc. have to be found and addressed for actual improvement to occur. By improvement, I mean not needing cortisol treatment.

Be that as it may, when iron stores are low (e.g. suboptimal ferritin) or other serious nutrient deficiencies are present, then adrenal function cannot be restored, intercellular signaling (e.g. thyroid signaling, etc.) can’t work well, etc. The primary problem is nutritional deficiency and cellular metabolic problems.

[hardasnails1973]

@DrMariano 755 wrote:

If cholesterol already is < 140 and LDL-cholesterol is already good, adjusting HDL cholesterol with Niacin may not be useful, and may instead cause side effect such as impaired concentration and memory. Cholesterol is an important component of cellular membranes. It makes up HALF of the dry weight of the brain. Lowering cholesterol production may instead worsen cellular metabolism and intercellular signaling. The most important target for reducing the risk of a heart attack is not cholesterol. It is inflammation. Without inflammation, high cholesterol does not lead to atherosclerotic plaque formation. When cholesterol is already low, targeting inflammation is far more useful than attempting to increase HDL-cholesterol. Reducing inflammation – such as by targeting excessive pro-inflammatory signaling – also helps reduce mood problems, cognitive problems, HPA Axis dysregulation, aches and pain, inflammatory diseases, etc. Cholesterol is synthesized from blood from sugars. Those who eat high animal protein, high saturated fat, high cholesterol meals actually have lower cholesterol than those who eat higher carb meals. A severely low carbohydrate diet can cause functional problems – unless one is on an Eskimo or Masai style total animal source diet. Carbs are necessary to help prevent the body from targetting proteins and amino acids as an energy source, for example. This may lead to amino acid deficiencies, and other imbalances, etc. When HPA Axis dysregulation is present, then carbohydrate intake can make a person fatigued. Excessive carbohydrate intake can shut down adrenal function, resulting in lower cortisol levels, which lowers gluconeogenesis. Once glucose normalizes after a carb meal, impaired gluconeogenesis results in low blood sugars (which to me is < 93). Adrenal support treatment using cortisol and DHEA alone is frequently a bandage treatment and won't reset HPA Axis regulation. The actual contributing factors - immune system overactivity, excessive pro-inflammatory cytokine signaling, stress, nutritional deficiencies, thyroid problems, etc. etc. have to be found and addressed for actual improvement to occur. By improvement, I mean not needing cortisol treatment. Be that as it may, when iron stores are low (e.g. suboptimal ferritin) or other serious nutrient deficiencies are present, then adrenal function cannot be restored, intercellular signaling (e.g. thyroid signaling, etc.) can’t work well, etc. The primary problem is nutritional deficiency and cellular metabolic problems.

Excessive zinc >50 mgs can also lower ferritin as it also competes in the intestinal tract with iron, manganese, copper, calcium.

By reducing excessive zinc this should help to rebalance other minerals, bring up ferritin levels. I also found a study that excessive iron in presence of low copper could result in inflammation with in the liver similar to hemochromatosis.

Could the inflammatory states one may look at would be potentially excesssive insulin production or signaling? My understanding is that excessive zinc consumption can produce a pro inflammatory response. After reading how important zinc is for the prostate one starts to take 50 mgs of zinc supplements. In a few months the BPH symptoms are lessen, but for the fear of the BPH returning that person continues to take >50 mgs a day indefinitely. Then all of sudden his symptoms start to return after about 6 months of continue supplementaton. It was later found out that he had been supplementing >50 mgs of zinc with out having proper copper balance. His blood report showed that his copper and ceruloplasmin levels dropped 30%, HDL were drastically reduced from baseline reading. The subject also noted hair getting dry and started to fall out, tingling and numbness in fingers and toes indicating slight neuropathy and delayed wound healing.

What markers can be used to intentify hidden inflammation since all my markers (CRP, c- peptide, LDL,insulin, Lp-PLA2, homocysteine).

If a glucose tolerance test was performed my insulin levels would probably be sky high or body may have an exaggerated response.

Last glucose tolerance test resulted in resting glucose of 80 and finishing up 3 hours later with 42. Unfortunately my insulin levels were never measured during this test. I never displayed signs of hypoglycemia during the test. The Dr was perplexed.

http://jn.nutrition.org/cgi/content/full/134/4/811
Zinc deficiency is a well-known health problem associated with delayed wound healing, yet the precise mechanisms that underlie the delay remain unknown. We hypothesized that zinc deficiency delays wound healing as a result of decreased nuclear factor (NF){kappa}B activation, reduced expression of proinflammatory cytokines [interleukin (IL)-1ß and tumor necrosis factor (TNF)-{alpha}], and a decrease in neutrophil infiltration during the early stage of cutaneous wound healing. We used a cutaneous, full-thickness excisional wound model in CD-1 mice to examine the rate of wound closure as well as mRNA levels of inhibitory (I){kappa}B{alpha}, IL-1ß, and TNF-{alpha} and infiltration of neutrophils at the wound site of mice fed a diet containing <1 (deficient), 50 (control), 500, or 1000 µg zinc/g diet. Zinc deficiency reduced the rate of wound closure and mRNA levels of IL-1ß and TNF-{alpha} and attenuated infiltration of neutrophils at the wound site compared with controls. Interestingly, zinc supplementation at 1000 µg/g delayed the rate of wound closure and decreased mRNA levels of TNF-{alpha} and infiltration of neutrophils compared with mice fed the control diet. These findings demonstrate that zinc deficiency and high-dose zinc supplementation delay wound healing as a result of altered inflammatory responses and suggest that adequate zinc supplementation may have beneficial effects on the inflammatory responses to enhance cutaneous wound healing.

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