Dr. Pickart,

Would it be safe for me to take copper supplements as a Type 1 diabetic? I've read that diabetics can have excess copper. Wanted to try supplementing as you suggested to improve my hair & skin.

Thank you.

There is a great deal of confusion in this area. 30 years ago, it was thought that copper caused many diseases. But by the 1990s, it was found that copper supplements would cure or correct many of these diseases. Plasma copper and ceruloplasmin were used to determine copper levels but were not useful because they are increased by inflammation and disease, and may be falsely high.

Also, may studies use free copper ion and not peptide or protein bound copper. For example, free copper oxidizes low density lipoproteins. GHK-copper blocks the oxidation of low density lipoproteins. There is essential no free ionic copper in the human body. It is all bound the GHK or proteins.

As for diabetes, additional supplemental copper reduces many of the biochemical problems associated with diabetes like excessive tissue oxidation and protein damaging glycations.

Metabolism. 2008 Sep;57(9):1253-61.
Oxidative stress in Cohen diabetic rat model by high-sucrose, low-copper diet: inducing pancreatic damage and diabetes.
Ryu S, Ornoy A, Samuni A, Zangen S, Kohen R.

Department of Anatomy and Cell Biology, Laboratory of Teratology, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.

Increased oxidative stress contributes to the development and progression of both types of diabetes mellitus (DM) and its complications. In the Cohen diabetic (CD) rats, a known genetic model of nutritionally induced type 2 DM, a high-sucrose, low-copper diet (HSD) induces within 4 weeks DM in the sensitive (CDs) rats but not in the resistant (CDr) rats. To assess the possible involvement of oxidative stress in the induction of DM, we studied the effect of HSD on the tissue levels of antioxidants and the extent of oxidative injuries in these animals in comparison with the regular outbred strain of nondiabetic Sabra rats. The specific aims were to investigate, at the onset of HSD-induced DM, (1) the extent of oxidative injury, as reflected by levels of malondialdehyde and protein carbonyl groups; (2) the overall antioxidant capacities to cope with increased oxidative stress; and (3) the modification of oxidative damage biomarkers in various tissues of CDr, CDs, and Sabra rats. Female CDs, CDr, and Sabra rats were fed regular diet or HSD for 4 to 5 weeks; and several parameters of oxidative injuries and antioxidant levels were determined. Changes in the levels of nonenzymatic low-molecular weight antioxidants (LMWAs) were measured by cyclic voltammetry and oxygen radical absorbance capacity. The activities of the antioxidant enzymes superoxide dismutase and catalase were measured. Oxidative damage was evaluated by measuring lipid peroxidation and protein oxidation. (1) In all animals fed HSD, the levels of LMWAs were decreased in most organs, although not plasma. (2) A significant difference was consistently found in antioxidant enzymes' activities in the pancreas of HSD-fed CDs rats, but not in other tissues. (3) The activities of superoxide dismutase and catalase and the levels of malondialdehyde and protein carbonyl group increased, whereas the levels of LMWAs decreased, in the pancreas of HSD-fed CDs rats. In the CD rats that develop DM when fed HSD, the pancreas showed susceptibility to oxidative stress-induced injuries. Thus, enhanced oxidative stress seems to play a role in the pathogenesis of DM in this strain.

Environ Health Perspect. 2007 July; 115(7): A341–A342.

Copper Deficiency, Lead, and Paraoxonase
Leslie M. Klevay
University of North Dakota, School of Medicine and Health Sciences, Grand Forks, North Dakota, E-mail: leslie_klevay@und.nodak.edu

Li et al. (2006) measured paraoxonase 1 (PON1) in workers and found an inverse association between lead exposure and enzyme activity. This observation compliments some epidemiology and related experiments with animals, because low paraoxonase activity is associated with diabetes mellitus, familial hypercholesterolemia, ischemic heart disease, and metabolic syndrome (Klevay 2004). Paraoxonase, although studied most extensively because of its ability to detoxify organophosphate insecticides (James 2006; van Himbergen et al. 2006), has drawn increasing attention because it hydrolyzes homocysteine thiolactone, a vascular toxin that inhibits copper enzymes (Klevay 2006).
Lead intoxication has many manifestations (Fischbein 1998), lesser-known of which is induction of copper deficiency (Klauder and Petering 1977). Rats deficient in copper have an approximately 28% decrease in paraoxonase activity (Klevay 2004). These observations are consonant with the decrease in superoxide dismutase (SOD) associated with occupational exposure to lead (Ito et al. 1985) because this enzyme also depends on adequate copper nutriture for activity (Linder and Goode 1980; Owen 1981). Thus, SOD is an index of copper nutriture in humans (Uauy et al. 1985).
Li et al. (2006) stated that “the mechanism by which heavy metals inhibit serum PON1 activity is still not clear.” It seems likely that lead interferes with copper utilization in the workers, leading to low copper nutritional status (Li et al. 2006). Low copper status has been related to a large variety of adverse cardiovascular phenomena in both animals and people; in this context, the most important are hypercholesterolemia, hypertension, and impaired oxidative defense (Klevay 2000, 2002).
Are there unpublished copper data on the workers, or can they be reexamined to test this copper hypothesis? Plasma copper and ceruloplasmin are not likely to be useful because they are increased by inflammation (Pepys 1996) and may be falsely high. Extracellular SOD may be helpful because it is sensitive to low copper status (Johnson et al. 2005), and low values have been associated with atherosclerosis in humans (Landmesser et al. 2000; Wang et al. 1998).


from http://www.acemagnetics.com/ed...bracelets-aging.html

Can Copper Status Affect Aging?
Author/s: Judy Mcbride

Agricultural Research
August, 1999

Could a marginal intake of the essential element copper contribute to the aging process? ARS physiologist Jack T. Saari thinks that's a strong possibility--based on rat studies, along with a good bit of indirect evidence.

Saari and a colleague, chemist Gwen Dahlen, at the Grand Forks Human Nutrition Research Center in North Dakota wanted to see if copper deficiency spurs sugar molecules to attach to proteins. The process--nonenzymatic glycosylation, or protein glycation for short--is a spontaneous binding of sugar to protein without the aid of enzymes. It is thought to cause much of the tissue damage in people with diabetes. And it increases in all of us as we age, Saari says.

Tiny sugar molecules attached to a huge protein molecule may be likened to fleas on a dog. But the attached sugars can be more than annoying; they can be deadly to the protein. That's because their free ends tend to hook up to other proteins or other sites on the same protein, forming cross-links. These cross-links bend the protein out of shape so that it no longer functions properly. The useless protein soon gets degraded and hauled off for recycling or disposal.

In the early 1980s, Saari's colleague, Leslie M. Klevay, M.D., reported that copper-deficient rats had glycated hemoglobin--the oxygen-carrying molecule in red blood cells. Klevay heads the Mineral Nutrient Requirements Unit at Grand Forks.

Saari says this and more recent indirect evidence led him to look for a connection between copper deficiency and protein glycation.

Two pieces of indirect evidence come from studies at ARS' Beltsville (Maryland) Human Nutrition Research Center, as well as Saari's laboratory. Rats fed copper-deficient diets have high blood sugar, says Saari. This raises the odds for glycation.

"Their condition is like type-II diabetes," says Meira Fields, who conducted the Beltsville studies. Unlike Saari, Fields finds that the copper-deficient rats exhibit high blood sugar only when their diets are high in sugar--either fructose or sucrose. This sugar-laden diet also causes the rats to secrete less insulin, she says, which is needed to move sugar out of the blood and into the cells to serve as fuel.

What's more, Fields' studies have repeatedly shown that rats suffer the most tissue damage from this diet when the sugar is fructose. Saari notes that in the test tube, fructose is a better glycator than glucose.

Two more pieces of indirect evidence come from Saari's own studies. He reduced the symptoms of copper deficiency--such as an enlarged heart--by two different treatments. First, he fed the rats only a portion of the food they would normally eat. This kept blood glucose levels low, he says, reducing the chance of glycation. Second, he treated the rats with a chemical--aminoguanidine--known to block advanced glycation or cross-linking of sugars. And it worked.

Fractured Proteins

Armed with this evidence, Saari and Dahlen designed a study to look directly for increases in protein glycation. The results bore out their suspicions. Both the early and advanced stages of protein glycation increased significantly in the rats fed a copper-deficient diet.

One sensitive indicator of advanced glycation is a measure of the proteins that it has rendered ineffective. This indicator was at least six times higher in the copper-deficient rats. It was nearly undetectable in the control rats, he says, noting that Dahlen made this very delicate analysis possible by refining an existing analytical method. They published their findings in the April 1999 issue of the Journal of Nutritional Biochemistry.

Treating the rats with aminoguanidine did not reduce cross-linking in this study as it did in the earlier one, says Saari, probably because the dosage was too low. So he and Dahlen did a follow-up Study using a higher dosage. The earliest results available at this writing are showing a reduction in glycation caused by copper deficiency.

Copper Intake Lags

Humans consume more copper than rats do. But the average copper content of diets in the United States, Canada, Great Britain, and Belgium still falls below the U.S.-suggested intake range of 1.5 to 3 milligrams per day.

Klevay, a physician, pulled together data from the chemical analyses of 849 diets in the four countries. He says they show that 61 percent contained less than 1.5 mg of copper daily, and nearly a third of the diets provided less than 1 mg.

"That's in the range that has proved insufficient for both men and women in controlled dietary experiments," he says.

Vegetarian diets had more copper than nonvegetarian diets. That's because nuts, seeds, mushrooms, whole grains, and legumes--such as soybeans, peas, chickpeas, lentils, and peanuts--are good sources of the mineral. The richest sources of copper are animal--oysters, crabs, and liver--which are not common in the daily diet.

Estimated copper intake in the United States, based on USDA's latest nationwide food consumption survey, averages 1.2 mg/day for all individuals--below the 1.5 mg suggested minimum. The estimates show men averaging just the minimum 1.5 mg/day, while women average only 1 mg/day.

Saari speculates that years of eating a diet low in the mineral may be a factor contributing to the age-related decline in tissue function from increasing protein glycation.

"It's a low-grade phenomenon," he says. "It's not like diabetes where blood glucose stays high after an overnight fast." Instead, he says, blood glucose peaks higher than normal after a meal--increasing glycation--but it doesn't stick around. "The only way you know this increase is happening is through a glucose tolerance test or a test of glycated hemoglobin."

The early stage of glycation--when the sugar first attaches to the protein--is reversible. As blood sugar drops, the sugar can detach. Once the cross-links are formed, however, they don't come apart, Saari says. So far, he has looked only at glycation of hemoglobin and serum proteins. But it can also happen to structural proteins that form tissues.

Copper and Oxidation

The most accepted theory of aging holds that it results from cumulative damage to tissues by oxygen free radicals. These radicals are generated during normal metabolism and delivered by environmental pollution. Saari says his thesis fits hand in glove with the oxidation theory because glycation appears to increase oxidation.

According to reports in the diabetes literature, both free and attached sugar molecules can convert the benign oxygen molecule into a free radical. What's more, glycated proteins are more vulnerable to oxidation.

Copper is important to the body's defense against oxidation through a copper-containing enzyme--superoxide dismutase, or SOD. Saari notes that SOD activity reportedly decreases with aging, while oxidative damage increases.

Over the long term, a low copper intake could plausibly weaken this inherent antioxidant defense, slightly elevate blood sugar, and increase attachment of sugar to proteins--all of which tend to increase oxidative damage.

This research is part of Human Nutrition Requirements, Food Composition, and Intake, an ARS National Program described at http://www.nps.ars.usda. gov/programs/appvs.htm.

Jack T. Saari and Leslie M. Klevay are at the USDA-ARS Grand Forks Human Nutrition Research Center, P O. Box 9034, University Station, Grand Forks, ND 58202; phone (701) 795-8353, fax (701) 795-8395, e-mail jsaari@gfhnrc. ars.usda.gov.

This message has been edited. Last edited by: Dr. Pickart,

Thank you so much, Dr. Pickart.

May I have your permission to post this on a diabetes forum I belong to?

Do you think your copper peptides would be helpful in removing scar tissue on injection sites? It can be pretty serious thick scar tissue. I wanted to mention this as well on the forum.

Yes, you can post this.

The copper peptides activate skin remodeling which is the process that removes scar tissue and blemishes.

This is our general advice on scar reduction.

We think almost any skin blemish (scars and pitted scars, keratosis,
skin tags, moles, age spots, sun damage, stretch marks, warts,
hyperpigmentation and hypopigmentation, white scars, discoloration) can
be reduced or removed with a combination of hydroxy acids, skin
abrasion, and Skin Remodeling Copper Peptides (SRCPs).

The hydroxy acids and abrasive methods slowly loosen and dissolve the
blemish tissue and the SRCPs help the rebuilding of new skin.(Caution:
This advice applies only to normal skin blemishes. Any skin blemish that
appears dark, irregular, or bleeds should be promptly checked by a
dermatologist.)

Scar reduction is a balancing act of scar removal and rebuilding skin.
Too rapid removal of scar tissue and you get a hole in your skin and
too little scar removal and there is no progress. In the past,
dermatologists often observed that strong hydroxy acids, and other
methods like the use of liquid nitrogen on blemishes, would remove the
skin blemishes but subsequent skin irritations limited the use of these
methods.

Skin may look worse for a time during scar reduction. Some deep scars
such as from acne are covered over with a layer of good skin but as
the buried scar tissue is pushed to the surface, it becomes
noticeable. Often, one has to first get the skin into a healthier
condition and then focus on removing the scars. More SRCPs makes skin
healthier, more hydroxy acids remove tissue. The method is slow but
usually works and has no downside.

We find that repeated use of moderate strength hydroxy acid, followed
by the use of SRCPs, usually removes skin blemishes without excess
skin irritation.

The SRCPs are usually rubbed into the scar area in the morning and the
Hydroxy acid product rubbed in at night. Stronger hydroxy acids and our
stronger SRCPs work faster but irritation can sometimes be a problem
with the stronger products. Sometimes, people also use retinoic acid
(Retin-A or Renova) along with the hydroxy acids to speed scar removal.
The products should be used every day.

Some people with severe scars have had good results by applying the
products four times daily a hydroxy acid at 8 am, a SRCP at noon, a
hydroxy acid at 5 PM, and a SRCP before bedtime. You should see an
improvement in a month but some old scars such as stretch marks and
keloid scars may take 6 to 8 months to slowly
remove. Slower is better in scar reduction.

1.If you are under 30, have acne in the scar area, or have rosacea,
then use Super CP Serum in the morning and LacSal Serum at night.
Start the products lightly - 1 drop of each daily then slowly
increase the amount used.

2.If acne is not a problem, then use TriReduction Cream in
the morning and LacSal cream at night.

3.If you are not getting enough effect, then try Super Cop or Super
Cop 2X Extra Strength Extra which are our strongest SRCP but can cause
itching. If it itches, you can wash it off with warm water. Skin
slowly adapts to the Super Cops but this can take some time.
Usually Super CP Serum is applied lightly in the AM ( 3-4 drops to the
entire face) and concentrated specifically on your areas of concern. A
Super Cop Cream (or Super Cop 2X) can be used as a spot treatment once
a day very lightly. You can even work it into the skin with a flat
toothpick.

4.Some clients report good results after applying Super CP Serum,
letting it dry for a short time, then applying LacSal Cream over the
Super CP Serum.

5. If you still are not getting a good enough effect, then replace our
hydroxys with a 30% glycolic acid or lactic acid product. There are
links to sellers of these at www.scar-reduction.com or
http://www.reverseskinaging.com/resellers.html. For difficult lesions,
like age spots, the salicylic acids (about 12% salicylic acid) used for wart
and callus removal often work well - drugstores have these.

6. Skin color usually reverts to its pre-damage color.

7. Blemish reduction can be further accelerated by skin abrasion with
exfoliating washclothes (microdermabrasion cloths), pumice stones,
abrasive pads, or microdermabrasion kits such as those used to remove
calluses. Flat toothpicks can loosen pitted scar tissue. Subcision
with needles is often also used to break up hard or fat containing scar
tissue in depressed scars such as after cystic acne.

A product called Dermaroller (roller with needles) is often reported to
work well with our copper peptides. It is available on Internet. Don't
use it more than once weekly. Clean it after use and sterilize it before
further use.

8.Using Retinoic acid (Renova or Retin-A) with SRCPs often produces
faster scar reduction. Use 0.25% to 0.50% retinoic acid creams which
are strong.

9.Daily supplements of 1 gram vitamin C, 1 gram MSM, and 1 gram each
of either flaxseed oil, borage oil, or primrose oil also help skin
rebuilding.

10.Stress inhibits skin repair and the rate of scar reduction by
increasing blood cortisol. Taking 75 to 100 mgs daily of DHEA during
periods of high stress may help block the cortisol effect and
stimulate skin repair.

11.Regular aerobic exercise floods more blood into the skin and
speeds skin repair and scar reduction.

12. There is more information at www.scar-reduction.com.

Thank you, Dr. Pickart. Grateful for your help & for the wonderful products!

Alpha lipoic acid is widely used in Europe for preventing damage during diabetes.

I've been taking ALA. It's supposed to help lower insulin requirements also, but I haven't noticed an effect yet. I may need to increase the dose. I've read that it often takes quite a bit. Thank you for mentioning ALA.

I read your copper supplementation info, but am confused as to recommended dosage, other than the ratio of zinc to copper. Could you please tell me how much to take? Is it better to take zinc & copper at different times as wll?

Thank you.

What kind of copper supplements would you recommend for diabetics? Are there any specific ones you know of. Being an insulin dependent diabetic, I have always found the world of nutrition to be a mindfield of info and thank goodness I have avoided the complications associated with diabetes for such a long time and wish to keep it that way, and hey if copper as a supplement can help - the more the better I'm thinking!

I took ALA as well, for a very long time, and although you might not notice an immediate effect, it takes a while for the body to become accustomed to using it. I think the ultimate thing to try with regards to insulin is chromium, as that really does it for many diabetics but its long term studies have never really been carried out as of yet.

On many of the websites I have read about dermarolling - they always advise diabetics not to use it as a tool. I thought this was partly because of the impaired ability to recuperate from skin cuts etc, but it never made sense to me - but its one of the main things putting me off from using one. I suppose one day I will - but be interested to hear Dr Pickart's thoughts on how a dermaroller won't impact diabetics adn their skins?

quote:

A product called Dermaroller (roller with needles) is often reported to
work well with our copper peptides. It is available on Internet. Don't
use it more than once weekly. Clean it after use and sterilize it before
further use.

People with diabetes do heal more slowly. The real risk is infecting the skin.

If you use a dermaroller, use a short needle and make certain that the unit is sterile.

quote:

Originally posted by SeanySeanUK:
What kind of copper supplements would you recommend for diabetics? Are there any specific ones you know of. Being an insulin dependent diabetic, I have always found the world of nutrition to be a mindfield of info and thank goodness I have avoided the complications associated with diabetes for such a long time and wish to keep it that way, and hey if copper as a supplement can help - the more the better I'm thinking!

I took ALA as well, for a very long time, and although you might not notice an immediate effect, it takes a while for the body to become accustomed to using it. I think the ultimate thing to try with regards to insulin is chromium, as that really does it for many diabetics but its long term studies have never really been carried out as of yet.

No one really knows what we should take. Many researchers on copper and health take 4 mgs of chelated copper. At a ratio of 7 to 1, zinc to copper, this would mean also to take 28 mgs of zinc daily.

Great thank you Dr Pickart - this is helpful!

SeanySeanUK,

What dose of ALA did you take & for how long? Are you not taking this any more?

Thanks!

I was taking the Viridian Supplement of ALA, which was recommend to me by my dietian, and I took it for about 4 months and didn't feel any noticeable benefits to it, however thats probably not long enough. However when I have taken things like EPA Marine Oil or the right Vit C, I feel very different within hours of taking it, almost energetic and healthier (and its probably mostly a psychological response - but hey its all worth it).

One thing that I noticed that really did help me with both sugar and insulin was chromium, but the first two supplements I tried just weren't for my body, but the third - wow. It really helped me lower my insulin levels somewhat which was great.

Loved to know which copper supplement products your trying and what the results are going to be like! Please, please keep me posted!

People who do research on copper usually take 4 mgs as a copper amino acid complex (copper-glycinate for example) or a copper peptide complex.

As for the other supplements, take what works for yourself. This is always a slow search to find what you need. For many years I had migrane headaches (like my mother and grandmother). 4 grams of salmon oil daily totally stopped the headaches.

Dr Pickart,

What is your opinion of megadosing with biotin supplements with respect to speeding hair and skin growth?