An article in this month's (May 2013) American Journal of Medicine shows that current users of marijuana have better glucose control than do former users, who in turn have better glucose control than do abstainers. This study was a retrospective one, and needs to be validated by a forward study. This will probably never happen, for obvious reasons, much as retrospective studies showing that cigarette smokers have a lower incidence of Parkinson's disease were never followed up.
The use of marijuana was based on interviews with the 4657 members of the study; of this group 579 were current users and 1975 were prior users. Fasting glucose and insulin levels were measured, and the degree of insulin resistance was calculated. Diabetics and pre-diabetics both have insulin resistance.
This study was triggered by prior studies showing that marijuana users have a lower incidence of both obesity and diabetes, but there have been no similar studies of THC users. Current marijuana users in this study were seen to have lower levels of fasting insulin, and were less likely to be insulin resistant. They also had higher levels of HDL cholesterol and smaller waist sizes. Past users (more than 30 days before the study questionnaire) also had a lower incidence of insulin resistance than did non-users, but not as low as did current users.
The results of this study need to be followed up, but given the current federal law classifying marijuana as a Class I drug, meaning "no significant medical benefit", it is difficult to envision a prospective study being done. One possibility might be in the state of Washington or Colorado, where marijuana was recently legalized. OTOH, perhaps the federal law could be changed to make it legal to treat diabetes and the metabolic syndrome with THC and to do a study of its effect.
Friday, May 17, 2013
Sunday, May 12, 2013
The New Arabian Coronavirus.
A new respiratory virus which has killed 18 of the 31 infected cases has arisen in Saudi Arabia, where teams of Arabian physicians, members of the World Health Organization, and infectious disease specialists from the United States are all investigating jointly. This virus is a coronavirus, the same type (but genetically different) of the virus that originated in Chinses poultry and became the SARS virus when it infected man. The disease has developed in clusters of people. In one Arabian cluster of 15 people infected with the virus, 9 died. The most recent infection detected was in a man in France who inhabited the same hospital room as a person who returned from Dubai to France and was found to have the virus.
The virus has a predilection for elderly people with underlying chronic medical conditions that might impair their ability to fight disease. There is some evidence for people-to-people transmission, but this connection is weak and not 100%. For instance, only one doctor taking care of a patient has developed the disease. But since there are 4 clusters of the disease, this is evidence for weak person-to-person transmission.
At this point, we do not know the (presumed) animal reservoir of the disease. This disease has the potential to mutate and become much more infective and transmissible, which could create a weak epidemic or a strong pandemic. There is no antiviral currently on the market that treats this
infection, and efforts are just starting to sequence its genome and to develop a vaccine. There is not much more to say, except to recommending avoiding travels to areas in the Middle East where this new coronavirus has been found, as well as avoiding travels to areas of China and Taiwan where the new bird flu, InfluenzaA-N7H9 has been detected.
I strongly recommend following ProMED,com, the daily e-mailing of the International Society of Infectious Disease (ISID) for up to date information on both viruses.
The virus has a predilection for elderly people with underlying chronic medical conditions that might impair their ability to fight disease. There is some evidence for people-to-people transmission, but this connection is weak and not 100%. For instance, only one doctor taking care of a patient has developed the disease. But since there are 4 clusters of the disease, this is evidence for weak person-to-person transmission.
At this point, we do not know the (presumed) animal reservoir of the disease. This disease has the potential to mutate and become much more infective and transmissible, which could create a weak epidemic or a strong pandemic. There is no antiviral currently on the market that treats this
infection, and efforts are just starting to sequence its genome and to develop a vaccine. There is not much more to say, except to recommending avoiding travels to areas in the Middle East where this new coronavirus has been found, as well as avoiding travels to areas of China and Taiwan where the new bird flu, InfluenzaA-N7H9 has been detected.
I strongly recommend following ProMED,com, the daily e-mailing of the International Society of Infectious Disease (ISID) for up to date information on both viruses.
Monday, May 6, 2013
The New Asian Bird Flu
I thought I would share some facts with you about the new strain of influenza A H7N9, that has arisen in China and probably comes from birds, although we are not 100% certain of that. There has, as yet, been no evidence of people-to-people transmission (unlike SARS which infected health care workers). Furthermore, although this flu strain is resistant to amantadine, it is susceptible to oral oseltamovir (Tamiflu).
As of the end of April, there have been 126 confirmed cases in China, and 24 or 19% died. Older people are more susceptible to both catching the flu and succumbing to it, especially if they have a chronic health problem. Cases have been found in eight contiguous provinces in eastern China as well as in Beijing, Shanghai and Taiwan. China is making prodigious efforts to learn all it can about the flu and the birds' contribution to it. The flu has been found in some chickens and ducks, but the flu virus is harmless to poultry, and birds who are infected with the virus show no signs of being ill.
Thankfully, in the over 1500 close contacts of sick patients there has been no evidence of the flu, so unless it mutates there is no risk of an epidemic or pandemic. Except for one pigeon, the virus has only been found in chickens and ducks for sale in marketplaces; farms seem to be exempt. Relatively few poultry are carrying the virus, and 20% of the people with the virus report no exposure to birds. Chinese physicians and technicians are making herculean efforts to track and to find the virus, as well as sequencing its genome, and are examining pigs as well as poultry.
China has invited members from the World Health Organization as well as from our own Center for Disease Control to come and assist in their work. In addition, the CDC is monitoring patients here in the US for cases of Influenza A/H7N9, but so far have found no cases. There is not even the suggestion of facts or cases being hidden by China, so whatever you read should be accepted.
In summary, the virus is mild and relatively rare in poultry, but has a case fatality rate of 20% in humans, and while we think that poultry is the reservoir, we are not yet sure.
As of the end of April, there have been 126 confirmed cases in China, and 24 or 19% died. Older people are more susceptible to both catching the flu and succumbing to it, especially if they have a chronic health problem. Cases have been found in eight contiguous provinces in eastern China as well as in Beijing, Shanghai and Taiwan. China is making prodigious efforts to learn all it can about the flu and the birds' contribution to it. The flu has been found in some chickens and ducks, but the flu virus is harmless to poultry, and birds who are infected with the virus show no signs of being ill.
Thankfully, in the over 1500 close contacts of sick patients there has been no evidence of the flu, so unless it mutates there is no risk of an epidemic or pandemic. Except for one pigeon, the virus has only been found in chickens and ducks for sale in marketplaces; farms seem to be exempt. Relatively few poultry are carrying the virus, and 20% of the people with the virus report no exposure to birds. Chinese physicians and technicians are making herculean efforts to track and to find the virus, as well as sequencing its genome, and are examining pigs as well as poultry.
China has invited members from the World Health Organization as well as from our own Center for Disease Control to come and assist in their work. In addition, the CDC is monitoring patients here in the US for cases of Influenza A/H7N9, but so far have found no cases. There is not even the suggestion of facts or cases being hidden by China, so whatever you read should be accepted.
In summary, the virus is mild and relatively rare in poultry, but has a case fatality rate of 20% in humans, and while we think that poultry is the reservoir, we are not yet sure.
Tuesday, April 9, 2013
Red Meat, Carnitine, and ASCVD
There was a recent article published in Nature Medicine that was picked up by the wire services and made its way into the mainstream media, including both the NY Times and the Wall Street Journal. Many readers have asked me to comment on the report. In what follows, again please remember that correlation or association is not causation.
The article cited studies of 2950 patients undergoing cardiac evaluation, and found that increasing levels of carnitine correlated positively with the risk for stroke and heart attacks. Gut bacteria can convert carnitine to a compound called TMAO, and levels of this compound have been correlated with atherosclerosis in the past.In mice, TMAO inhibits the breakdown of cholesterol. Due to the absence of meat in their diet, vegetarians have much lower levels of carnitine than do meat eaters.
Based on other studies, TMAO may promote the growth of plaques in arteries, but the data is not solid. At this point, we do not know if there is a third molecule derived from TMAO that is also correlated with cardiovascular events.
L-carnitine (carnitine is a stereo isomer and comes in both an l (left-handed) and d (right-handed) form, but as is usual with the human body, our enzymes recognize only the l form of amino acids. L-carnitine is a facilitator for the cell's use of fatty acids to obtain energy with the help of vitamin C via the citric acid cycle. The body can make carnitine as well as obtain it from food, which is not surprising since it is a necessary part of the energy cycle, and children born without the ability to use carnitine suffer severe metabolic problems.
The body has other uses for carnitine, and I will discuss a few. It has been shown in clinical studies that administering l-carnitine to patients with angina reduces the amount of cardiac medicine they need, and increases their chest pain-free exercise ability. The amount of carnitine in cells decreases with age, which thereby diminishes osteocalcin which in turn promotes osteoporosis.
Oddly enough, one study suggested that carnitine can improve sperm quality in infertile men, and can also reduce the size of a variocele.
Carnitine reduces fat mass and increases muscle mass, which is why bodybuilders take so much of it. Carnitine supplements appear to improve neurotransmitter functioning in the brain of elcerly patients. It was also found that l-carnitine levels were lower in children with asthma, and administering l-carnitine to these asthmatic children improved their pulmonary function tests. L-carnitine is also a peripheral antagonist of thyroid hormone action.
To summarize, increased l-carnitine levels in patients with increased TMAO levels was positively correlated with cardiovascular events, and further studies are definitely needed.
The article cited studies of 2950 patients undergoing cardiac evaluation, and found that increasing levels of carnitine correlated positively with the risk for stroke and heart attacks. Gut bacteria can convert carnitine to a compound called TMAO, and levels of this compound have been correlated with atherosclerosis in the past.In mice, TMAO inhibits the breakdown of cholesterol. Due to the absence of meat in their diet, vegetarians have much lower levels of carnitine than do meat eaters.
Based on other studies, TMAO may promote the growth of plaques in arteries, but the data is not solid. At this point, we do not know if there is a third molecule derived from TMAO that is also correlated with cardiovascular events.
L-carnitine (carnitine is a stereo isomer and comes in both an l (left-handed) and d (right-handed) form, but as is usual with the human body, our enzymes recognize only the l form of amino acids. L-carnitine is a facilitator for the cell's use of fatty acids to obtain energy with the help of vitamin C via the citric acid cycle. The body can make carnitine as well as obtain it from food, which is not surprising since it is a necessary part of the energy cycle, and children born without the ability to use carnitine suffer severe metabolic problems.
The body has other uses for carnitine, and I will discuss a few. It has been shown in clinical studies that administering l-carnitine to patients with angina reduces the amount of cardiac medicine they need, and increases their chest pain-free exercise ability. The amount of carnitine in cells decreases with age, which thereby diminishes osteocalcin which in turn promotes osteoporosis.
Oddly enough, one study suggested that carnitine can improve sperm quality in infertile men, and can also reduce the size of a variocele.
Carnitine reduces fat mass and increases muscle mass, which is why bodybuilders take so much of it. Carnitine supplements appear to improve neurotransmitter functioning in the brain of elcerly patients. It was also found that l-carnitine levels were lower in children with asthma, and administering l-carnitine to these asthmatic children improved their pulmonary function tests. L-carnitine is also a peripheral antagonist of thyroid hormone action.
To summarize, increased l-carnitine levels in patients with increased TMAO levels was positively correlated with cardiovascular events, and further studies are definitely needed.
Sunday, April 7, 2013
Interpreting Medical Clinical Studies
It occurred to me that with so many reports of clinical studies quoted in the news, I should review this topic, or, rather, supplement my earlier blog which discussed the difference between absolute and relative risk, or the validity of a verbal report as compared to a published journal article, among other topics.
Let me begin by re-emphasizing that correlation is not causation, so that if people with disease A do or do not ingest substance B on a regular basis, this does not necessarily mean that you can reduce your risk of disease A by ingesting or refraining from substance B. However it is fair to say that if every study shows a correlation,(such as between smoking and lung cancer) then there probably is a causal relationship, bearing in mind that it is still possible that there is a common denominator of which we are unaware that links A and B. The classic example is the correlation between coffee drinking and coronary artery disease, where the confounding effect was that coffee drinkers were more likely to be smokers.
There are two classic errors that can occur in a clinical study. A type I error is when the scientist mistakenly believes that the intervention has an effect on the incidence of the disease. A type II error is when the scientist mistakenly believes that the intervention has no effect. Most studies are designed to minimize and accurately define the chance of a type I error, and a positive study is generally statistically accepted if the probability of a type I error is less than 5%. This means that there is one chance in twenty that the conclusion is wrong, which is why I tell my patients to wait for a second prospective study. The chance of a type I error can never be zero. A type II error is directly related to the square root of the number of people in the study, so that by including enough patients, the likelihood of a type II error can be made as small as you like (at an additional expense and inconvenience to the observer).
There are two types of studies: retrospective and prospective. A retrospective study interviews people with disease A and compares the results with a matched set of individuals (matched as to age, sex, race, and/or other qualities as closely as possible). The study then tries to find differences in their past history between the two groups: did they go to graduate school, do they exercise, do they take Vitamin E, or whatever the scientist feels like studying. It is statistically fairer and more rigorously accurate if you specify in advance what action you are studying, rather than just do a blanket survey for differences. By the laws of chance, you are guaranteed to make a type I error if you survey all interventions. To be called an accurate marksman you must specify which leaf on the tree you are trying to hit before you fire a bullet into its branches and see that you hit a leaf.
A prospective study can be defined so as to accurately calculate the chance of a type I or type II error. In this study, we take a matched set of patients, do intervention B on one set, and compare the incidence of disease A in both sets after a fixed time period, which may be as long as five years for a dietary intervention, and as short as 30 days if we are looking for the occurrence of a second heart attack after the first one. In this case we have definitely defined both the intervention and the disease for which we are looking.
Most of the medical news with which we are bombarded has to do with retrospective studies, and we are assailed with the information that intervention A is good or bad for you based on them. A retrospective study should only be used to suggest a hypothesis, which then should be tested by a prospective study. Any retrospective study is filled with pitfalls, beginning with relying on the subject's memory of what he or she did or didn't do, e.g. the number of aspirin you took per week, on the average, over the past five years. And then we have headlines such as "more coffee drinkers get pancreatic cancer" (subsequently shown to be untrue). But since every retrospective study shows that adult females who drink two or more cups of coffee a day have a lower incidence of adult onset diabetes, there probably is a causative link between the two.
Be especially wary of the statement that more people who live in a certain area have more or less than the nationwide incidence of a disease. By the laws of statistics, the population of most counties or cities will have either more or less than the national average of almost everything. We don't even have consistent results comparing the lifespans of taller and shorter people, or right-handed people to left-handed people.
When I read about the results of a retrospective study, I say to myself "Very interesting. I wonder what a prospective study would show". It has been my experience that most retrospective conclusions are not validated by the ensuing prospective study, and very often a second prospective study does not agree with the first. Lancet had back-to-back articles with opposite conclusions as to whether or not a low salt diet prevented hypertension.
One last point. Often it is noticed that people with a certain medical problem (e.g. ASCVD) have an abnormal test (such as the CRP). We then jump to the erroneous conclusion that lowering the CRP will reduce the incidence of coronary artery disease, which conclusion has never been validated. My analogy to this is that pulling down on the metal floor indicator in the lobby of an office building will not bring the elevator down.
Let me begin by re-emphasizing that correlation is not causation, so that if people with disease A do or do not ingest substance B on a regular basis, this does not necessarily mean that you can reduce your risk of disease A by ingesting or refraining from substance B. However it is fair to say that if every study shows a correlation,(such as between smoking and lung cancer) then there probably is a causal relationship, bearing in mind that it is still possible that there is a common denominator of which we are unaware that links A and B. The classic example is the correlation between coffee drinking and coronary artery disease, where the confounding effect was that coffee drinkers were more likely to be smokers.
There are two classic errors that can occur in a clinical study. A type I error is when the scientist mistakenly believes that the intervention has an effect on the incidence of the disease. A type II error is when the scientist mistakenly believes that the intervention has no effect. Most studies are designed to minimize and accurately define the chance of a type I error, and a positive study is generally statistically accepted if the probability of a type I error is less than 5%. This means that there is one chance in twenty that the conclusion is wrong, which is why I tell my patients to wait for a second prospective study. The chance of a type I error can never be zero. A type II error is directly related to the square root of the number of people in the study, so that by including enough patients, the likelihood of a type II error can be made as small as you like (at an additional expense and inconvenience to the observer).
There are two types of studies: retrospective and prospective. A retrospective study interviews people with disease A and compares the results with a matched set of individuals (matched as to age, sex, race, and/or other qualities as closely as possible). The study then tries to find differences in their past history between the two groups: did they go to graduate school, do they exercise, do they take Vitamin E, or whatever the scientist feels like studying. It is statistically fairer and more rigorously accurate if you specify in advance what action you are studying, rather than just do a blanket survey for differences. By the laws of chance, you are guaranteed to make a type I error if you survey all interventions. To be called an accurate marksman you must specify which leaf on the tree you are trying to hit before you fire a bullet into its branches and see that you hit a leaf.
A prospective study can be defined so as to accurately calculate the chance of a type I or type II error. In this study, we take a matched set of patients, do intervention B on one set, and compare the incidence of disease A in both sets after a fixed time period, which may be as long as five years for a dietary intervention, and as short as 30 days if we are looking for the occurrence of a second heart attack after the first one. In this case we have definitely defined both the intervention and the disease for which we are looking.
Most of the medical news with which we are bombarded has to do with retrospective studies, and we are assailed with the information that intervention A is good or bad for you based on them. A retrospective study should only be used to suggest a hypothesis, which then should be tested by a prospective study. Any retrospective study is filled with pitfalls, beginning with relying on the subject's memory of what he or she did or didn't do, e.g. the number of aspirin you took per week, on the average, over the past five years. And then we have headlines such as "more coffee drinkers get pancreatic cancer" (subsequently shown to be untrue). But since every retrospective study shows that adult females who drink two or more cups of coffee a day have a lower incidence of adult onset diabetes, there probably is a causative link between the two.
Be especially wary of the statement that more people who live in a certain area have more or less than the nationwide incidence of a disease. By the laws of statistics, the population of most counties or cities will have either more or less than the national average of almost everything. We don't even have consistent results comparing the lifespans of taller and shorter people, or right-handed people to left-handed people.
When I read about the results of a retrospective study, I say to myself "Very interesting. I wonder what a prospective study would show". It has been my experience that most retrospective conclusions are not validated by the ensuing prospective study, and very often a second prospective study does not agree with the first. Lancet had back-to-back articles with opposite conclusions as to whether or not a low salt diet prevented hypertension.
One last point. Often it is noticed that people with a certain medical problem (e.g. ASCVD) have an abnormal test (such as the CRP). We then jump to the erroneous conclusion that lowering the CRP will reduce the incidence of coronary artery disease, which conclusion has never been validated. My analogy to this is that pulling down on the metal floor indicator in the lobby of an office building will not bring the elevator down.
Sunday, March 31, 2013
Drug Reps and Doctors
Several non-physician readers have asked me questions about the relationship between drug reps and doctors, and between drug companies and doctors, so I thought I would set the record straight.
Firstly, the major cost decision is when the doctor decides that the patient needs a new drug, e.g. a statin to lower cholesterol. The variation in price between two brands (or two generics) is generally less than 10%. The major cost comes from the doctor's deciding to prescribe the drug, and the drug rep has little or no control over that. Whether the doctor prescribes Lipitor, or Crestor, or simvastatin depends on many facts, mostly upon what the doctor has read. If he/she feels there is no difference among the statins on the market, then the decision is almost a random one. The point here is that the best a drug rep can hope for is to get the doctor to prescribe a particular brand of a statin, and the price difference between brand A and brand B is as I have said, not large. Again, let me emphasize that the medical decision that the patient needs a certain class of drugs is the major decision influencing the cost to the patient. For instance, if the patient has atrial fibrillation, then anticoagulation to reduce the risk of a stroke is usually mandatory.
The drug reps are strictly limited by the FDA as to what information can be told to or given to the doctors. The rules are so strict that if a drug rep has highlighted a sentence in a journal article, then he/she can only hold the article up for me to read. It is forbidden to give me the article with highlighting because the FDA fears that drawing my attention to the highlighted sentence might unduly influence me. Another rule is that the drug company can only give as a gift an an article that a non-doctor has no use for. They can give me reflex hammers or tuning forks or pocket eye charts, but no coffee cups or ballpoint pens(!). And if I have a question about the side effects, etc. of a drug, every company has a doctor's hotline whereby I can request information from the company directly. Alternatively, I can file a request for more information with the drug rep.
The drug reps can invite the doctors to a dinner where another doctor is lecturing on the drug rep's drug. The slides are supplied by the drug company and the company's lawyers restrict the words the doctor can use. The doctor who gives the talk is paid for his/her speech but the other doctors are paid nothing, but the dinner is free.And doctors can no longer bring along their wives to the dinner, unless the wife also works in the office as an office manager, etc.
There is a service that sells to the drug companies a list of all the doctors in a given area along with the number of prescriptions of the company's product a doctor prescribes in one or three months. The speakers at the dinner are chosen from doctors who are the heaviest prescribers of the medicine on which they are asked to speak, so paying them for the talk is a post hoc decision, and does not induce the doctor to prescribe a drug that he/she already heavily prescribes. The drug company only hopes the lecture will influence other doctors to prescribe more of the drug. After the talk, the doctors are free to ask questions to the speaker.
Doctors who write published articles must post a disclaimer at the end of the article, listing all the drug companies for which they have given speeches, or been a consultant for, or received any remuneration from, so that readers are immediately made aware of any possible conflict of interest.
Firstly, the major cost decision is when the doctor decides that the patient needs a new drug, e.g. a statin to lower cholesterol. The variation in price between two brands (or two generics) is generally less than 10%. The major cost comes from the doctor's deciding to prescribe the drug, and the drug rep has little or no control over that. Whether the doctor prescribes Lipitor, or Crestor, or simvastatin depends on many facts, mostly upon what the doctor has read. If he/she feels there is no difference among the statins on the market, then the decision is almost a random one. The point here is that the best a drug rep can hope for is to get the doctor to prescribe a particular brand of a statin, and the price difference between brand A and brand B is as I have said, not large. Again, let me emphasize that the medical decision that the patient needs a certain class of drugs is the major decision influencing the cost to the patient. For instance, if the patient has atrial fibrillation, then anticoagulation to reduce the risk of a stroke is usually mandatory.
The drug reps are strictly limited by the FDA as to what information can be told to or given to the doctors. The rules are so strict that if a drug rep has highlighted a sentence in a journal article, then he/she can only hold the article up for me to read. It is forbidden to give me the article with highlighting because the FDA fears that drawing my attention to the highlighted sentence might unduly influence me. Another rule is that the drug company can only give as a gift an an article that a non-doctor has no use for. They can give me reflex hammers or tuning forks or pocket eye charts, but no coffee cups or ballpoint pens(!). And if I have a question about the side effects, etc. of a drug, every company has a doctor's hotline whereby I can request information from the company directly. Alternatively, I can file a request for more information with the drug rep.
The drug reps can invite the doctors to a dinner where another doctor is lecturing on the drug rep's drug. The slides are supplied by the drug company and the company's lawyers restrict the words the doctor can use. The doctor who gives the talk is paid for his/her speech but the other doctors are paid nothing, but the dinner is free.And doctors can no longer bring along their wives to the dinner, unless the wife also works in the office as an office manager, etc.
There is a service that sells to the drug companies a list of all the doctors in a given area along with the number of prescriptions of the company's product a doctor prescribes in one or three months. The speakers at the dinner are chosen from doctors who are the heaviest prescribers of the medicine on which they are asked to speak, so paying them for the talk is a post hoc decision, and does not induce the doctor to prescribe a drug that he/she already heavily prescribes. The drug company only hopes the lecture will influence other doctors to prescribe more of the drug. After the talk, the doctors are free to ask questions to the speaker.
Doctors who write published articles must post a disclaimer at the end of the article, listing all the drug companies for which they have given speeches, or been a consultant for, or received any remuneration from, so that readers are immediately made aware of any possible conflict of interest.
Monday, March 18, 2013
Calcium Supplements, Good or Bad?
There have been several articles recently published in medical journals (JAMA, New England Journal of Medicine, British Medical Journal) about the possible risks associated with taking calcium supplements. The study groups are respected researchers, and include our own National Institute of Health. The studies addressed only the question of calcium supplements, and not the impact on health of a diet that was high in calcium.
I must state in advance that one problem with the results of the studies, besides their contradictory results, is that we have no good explanation for their results. While this does not mean the results are not valid and true, this lack of reasoning as to cause and effect makes it more difficult to believe in the result. It is also puzzling why the two main studies found different effects in men and women, and the results of one contradicted the results of the other.
The amount of calcium in your blood is very closely controlled by the body, and it is the ionized calcium, Ca++, a divalent cation that is the active form. Calcium exists in your blood both free as a cation and bound to serum proteins, and the aforementioned studies did not measure calcium levels. Because magnesium also exists as a divalent cation it often precipitates out in laboratory processes along with calcium, which led to the belief that the use of a supplement that contained magnesium as well as calcium was beneficial; no such result has ever been shown to be valid. However, since calcium is mildly constipating and magnesium is a mild laxative, combining the two elements into one pill makes theoretical clinical sense. Strontium is also a divalent cation, and unfortunately can be taken up by your bones along with calcium, which explains some of the bone marrow cancers induced by the radioactive strontium fallout from an atomic explosion.
The calcium levels are controlled by parathyroid hormone, which also activates Vitamin D into its useful form and thereby promotes the uptake of calcium by your bones both directly and indirectly. As a rule, the amount of calcium in your diet does not affect the level of calcium in your bloodstream. It is generally agreed that the calcium in your diet should contain between 600mg to 1200mg of calcium daily, along with 400 Units of Vitamin D, in order to maintain bone strength and prevent osteoporosis because activated Vitamin D promotes the absorption of calcium from your gut. We also know that ingesting too much calcium if you have chronic kidney disease can promote calcification of the arteries in your body, probably because kidney failure induces a state of secondary hyperparathyroidism, but a further discussion of this condition is beyond the scope of this article. Parathyroid hormone also increases the absorption of phosphate from your intestine which makes clinical sense since the largest mineral constituent of your bones is hydroxylapatite, which contains both calcium and phosphorous.
Now as to the studies. The question asked was whether or not taking calcium supplements (1000 mg or more in men and 1400 mg or more in women) had a benefit on the patient's health. One study showed an increase in overall mortality, and cardiovascular mortality as well as in heart attacks, but not in stroke. This increase in mortality was shown to exist in men, but not in women. Another study, published at about the same time, showed a similar increase in overall and cardiovascular mortality in women, but not in men(!).In each study the control group was same-sex patients who did not take calcium supplements.
So what are we to believe? There even are no clear-cut studies showing that calcium supplements prevent osteoporotic fracture; in fact some studies show an opposite result. (But taking extra Vitamin D at a dose of 800 mg/day does seem to prevent such fractures.) It is difficult to recommend calcium supplements in view of the above quoted data. It would be useful to have a study that measured calcium levels in people having heart attacks were it not for the fact that no one knows whether or not a MI acutely affects calcium levels. And it would seem heartless to tell the patients to read all three studies and to make up their own minds. I think that because no study showed by clear-cut evidence that taking calcium supplements was beneficial for one's health, then the recommendation of the doctor should come down on not recommending calcium supplements, thereby combining two tenets of medicine: "first, do no harm" and "less is more".
I must state in advance that one problem with the results of the studies, besides their contradictory results, is that we have no good explanation for their results. While this does not mean the results are not valid and true, this lack of reasoning as to cause and effect makes it more difficult to believe in the result. It is also puzzling why the two main studies found different effects in men and women, and the results of one contradicted the results of the other.
The amount of calcium in your blood is very closely controlled by the body, and it is the ionized calcium, Ca++, a divalent cation that is the active form. Calcium exists in your blood both free as a cation and bound to serum proteins, and the aforementioned studies did not measure calcium levels. Because magnesium also exists as a divalent cation it often precipitates out in laboratory processes along with calcium, which led to the belief that the use of a supplement that contained magnesium as well as calcium was beneficial; no such result has ever been shown to be valid. However, since calcium is mildly constipating and magnesium is a mild laxative, combining the two elements into one pill makes theoretical clinical sense. Strontium is also a divalent cation, and unfortunately can be taken up by your bones along with calcium, which explains some of the bone marrow cancers induced by the radioactive strontium fallout from an atomic explosion.
The calcium levels are controlled by parathyroid hormone, which also activates Vitamin D into its useful form and thereby promotes the uptake of calcium by your bones both directly and indirectly. As a rule, the amount of calcium in your diet does not affect the level of calcium in your bloodstream. It is generally agreed that the calcium in your diet should contain between 600mg to 1200mg of calcium daily, along with 400 Units of Vitamin D, in order to maintain bone strength and prevent osteoporosis because activated Vitamin D promotes the absorption of calcium from your gut. We also know that ingesting too much calcium if you have chronic kidney disease can promote calcification of the arteries in your body, probably because kidney failure induces a state of secondary hyperparathyroidism, but a further discussion of this condition is beyond the scope of this article. Parathyroid hormone also increases the absorption of phosphate from your intestine which makes clinical sense since the largest mineral constituent of your bones is hydroxylapatite, which contains both calcium and phosphorous.
Now as to the studies. The question asked was whether or not taking calcium supplements (1000 mg or more in men and 1400 mg or more in women) had a benefit on the patient's health. One study showed an increase in overall mortality, and cardiovascular mortality as well as in heart attacks, but not in stroke. This increase in mortality was shown to exist in men, but not in women. Another study, published at about the same time, showed a similar increase in overall and cardiovascular mortality in women, but not in men(!).In each study the control group was same-sex patients who did not take calcium supplements.
So what are we to believe? There even are no clear-cut studies showing that calcium supplements prevent osteoporotic fracture; in fact some studies show an opposite result. (But taking extra Vitamin D at a dose of 800 mg/day does seem to prevent such fractures.) It is difficult to recommend calcium supplements in view of the above quoted data. It would be useful to have a study that measured calcium levels in people having heart attacks were it not for the fact that no one knows whether or not a MI acutely affects calcium levels. And it would seem heartless to tell the patients to read all three studies and to make up their own minds. I think that because no study showed by clear-cut evidence that taking calcium supplements was beneficial for one's health, then the recommendation of the doctor should come down on not recommending calcium supplements, thereby combining two tenets of medicine: "first, do no harm" and "less is more".
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