Is it fraud, or is it more political deception, abetted by the incompetence of “highly respected” medical journals? Or both.
How could a respected journal publish papers based on data of unknown provenance? Isn’t there anyone with even a half-decent bullshit meter at work at The Lancet? It’s not even bad journalism (and even bad journalism is long gone), and it should make anyone skeptical of anything and everything in a medical journal.
The WHO’s feckless bureaucracy failed here also and it has done no better sorting fact from fiction on anything for a long time now.
But this is all part and parcel of a medical establishment that still thinks poison saves lives based on studies rife with conflicts of interest and unreleased data and cut-short trials—there is nothing new here really—same modus operandi where medical ethics are strictly limited in scope when it comes to drug trials.
On its face, it was a major finding: Antimalarial drugs touted by the White House as possible COVID-19 treatments looked to be not just ineffective, but downright deadly. A study published on 22 May in The Lancet used hospital records procured by a little-known data analytics company called Surgisphere to conclude that coronavirus patients taking chloroquine or hydroxychloroquine were more likely to show an irregular heart rhythm—a known side effect thought to be rare—and were more likely to die in the hospital.
Within days, some large randomized trials of the drugs—the type that might prove or disprove the retrospective study’s analysis—screeched to a halt. Solidarity, the World Health Organization’s (WHO’s) megatrial of potential COVID-19 treatments, paused recruitment into its hydroxychloroquine arm, for example.
But just as quickly, the Lancet results have begun to unravel—and Surgisphere, which provided patient data for two other high-profile COVID-19 papers, has come under withering online scrutiny from researchers and amateur sleuths. They have pointed out many red flags in the Lancet paper, including the astonishing number of patients involved and details about their demographics and prescribed dosing that seem implausible. “It began to stretch and stretch and stretch credulity,” says Nicholas White, a malaria researcher at Mahidol University in Bangkok. Today, The Lancet issued an Expression of Concern (EOC) saying “important scientific questions have been raised about data” in the paper and noting that “an independent audit of the provenance and validity of the data has been commissioned by the authors not affiliated with Surgisphere and is ongoing, with results expected very shortly.”
...
The Lancet at least is trying to correct its ineptitude, so maybe its reputation can remain somewhat above that of tabloid trash talk journalism.
See my more detailed post on this BMJ article.
This caught my eye, since I engage in year-round strenuous activity, averaging 1000 KCal/day during training season, and at least 800 KCal/day on a 365-day average.
After several weeks of strenuous physical activity, serum magnesium can increase with no change in erythrocyte magnesium levels despite a reduction in mononuclear cell magnesium levels. The authors of a study concluded that the reduction in mononuclear cell magnesium content ‘reflects a reduction in exchangeable magnesium body stores, and the onset of a magnesium deficiency state’.
This study also indicates that just 6–12 weeks of strenuous physical activity can lead to magnesium deficiency. Another study concluded: ‘Serum and urinary magnesium concentrations decrease during endurance running, consistent with the possibility of magnesium deficiency. This may be related to increased demand in skeletal muscle’.
For some years now, I have been puzzled why my peak fitness comes around mid-May and then inexplicably tends to decline and/or I have puzzling periods of weakness—which makes no sense at all(not a rest issue). At that point I typically have done six double centuries and burned about 1500 KCal/day on average since January—way more than enough to deplete magnesium. My working theory is that in spite of a 3000 to 3500 calorie per day diet (more food intake = more magnesium), I push myself into magnesium deficiency.
This year was messed up with most events canceled, but even so, I have kept my activity level fairly high. So my recent feel-better findings after magnesium supplementation are consistent with that theory and with everything I ponder about the past ten years of strenuous activity.
You may be reacting to prior posts by thinking I’ve gone off the deep end of accusing doctors of medical malpractice and gross ignorance of nutrition and nutrition deficiencies. But I am being far too kind given the worldwide health crisis and horrible suffering caused by this appalling professional ineptitude.
And with COVID-19, I wonder just how many deaths are resulting from nutrient deficiences caused by less than optimal health which at least for magnesium deficiency is very easy to fix.
“First, do no harm”
Doctors as a rule do not test for magnesium deficiency (or use the wrong test if they do) and therefore do not treat it, and thereby undermine patient health. Moreover, baseline amounts are a minimum not enough for optimal health.
This failure is nothing short of medical malpratice, because it puts patients at high risk for hundreds of maladies including very serious ones like diabetes and cardiovascular disease, not to mention weakening the immune system. What is going on with modern medical doctors to allow this callously incompetent situation to continue?
Abtract — Because serum magnesium does not reflect intracellular magnesium, the latter making up more than 99% of total body magnesium, most cases of magnesium deficiency are undiagnosed. Furthermore, because of chronic diseases, medications, decreases in food crop magnesium contents, and the availability of refined and processed foods, the vast majority of people in modern societies are at risk for magnesium deficiency. Certain individuals will need to supplement with magnesium in order to prevent suboptimal magnesium deficiency, especially if trying to obtain an optimal magnesium status to prevent chronic disease. Subclinical magnesium deficiency increases the risk of numerous types of cardiovascular disease, costs nations around the world an incalculable amount of healthcare costs and suffering, and should be considered a public health crisis. That an easy, cost-effective strategy exists to prevent and treat subclinical magnesium deficiency should provide an urgent call to action.
... despite renal conservation, magnesium can be pulled from the bone (as well as muscles and internal organs) in order to maintain normal serum magnesium levels when intakes are low. Thus, a normal serum magnesium level does not rule out magnesium deficiency, which predisposes to osteopaenia, osteoporosis and fractures...
... in order to prevent chronic diseases, we need to change our mindset away from exclusively treating acute illness and instead focus more on treating the underlying causes of chronic diseases, such as magnesium deficiency.
There are two types of nutrient deficiencies, frank deficiencies (such as scurvy from ascorbic acid deficiency or goitre from iodine deficiency) and subclinical deficiencies (a clinically silent reduction in physiological, cellular and/or biochemical functions). It is the latter that is most concerning as it is hard to diagnose and predisposes to numerous chronic diseases. And while both result in negative health consequences, the former has obvious symptoms (hence frank deficiency), whereas the latter may have negative or variable health effects that are not so apparent (eg, vascular calcification). The evidence in the literature suggests that subclinical magnesium deficiency is rampant and one of the leading causes of chronic diseases including cardiovascular disease and early mortality around the globe, and should be considered a public health crisis.
...In other words, children are overfed and undernourished. One expert has argued that a typical Western diet may provide enough magnesium to avoid frank magnesium deficiency, but it is unlikely to maintain high-normal magnesium levels and provide optimal risk reduction from coronary artery disease and osteoporosis... In other words, most people need an additional 300 mg of magnesium per day in order to lower their risk of developing numerous chronic diseases. So while the recommended daily allowance (RDA) for magne- sium (between 300 and 420mg/day for most people) may prevent frank magnesium deficiency, it is unlikely to provide optimal health and longevity, which should be the ultimate goal.
...much of the population may not even be meeting the RDA for magnesium... around half (48%) of the US population consumes less than the recommended amount of magnesium from food... substantial number of people may be at risk for Mg deficiency, especially if concomitant disorders and/ or medications place the individual at further risk for Mg depletion... large percentage of Americans may be at risk of negative magnesium balance... since many individuals may be consuming below 320mg/day of magnesium, this poses a major public health threat.
...correlation between the low magnesium consumption in food and the prevalence of risk factors for ischaemic heart disease, such as hyperlipoproteinaemia, arterial hypertension and body weight.
...Hypomagnesemia is a relatively common occurrence in clinical medicine. That it often goes unrecognized is due to the fact that magnesium levels are rarely evaluated since few clinicians are aware of the many clinical states in which deficiency, or excess, of this ion may occur.
...Magnesium deficiency has been found in 84% of post- menopausal women...
...Magnesium deficiency can be present despite normal serum magnesium levels
... our normal range of serum magnesium is inaccurate and that serum magnesium levels at the lower end of normal likely suggest marginal magnesium deficiency. Indeed, ‘The magnesium content of the plasma is an unreliable guide to body stores: muscle is a more accurate guide to the body content of this intracellular cation...
...prevalence of normomagnesemic Mg deficiency in critically ill patients may be even higher (than 65%, my insertion) and may contribute to the pathogenesis of hypocalcemia, cardiac arrhythmias and other symptoms of Mg deficiency.
...Hypomagnesemia detected at the time of admission of acutely ill medical patients is associated with an increased mortality rate for both ward and medical ICU patients’. Magnesium depletion is present in about half of all ICU patients...
This perception is probably enforced by the common laboratory practice of highlighting only abnormal results. A health warning is therefore warranted regarding potential misuse of ‘normal’ serum magnesium because restoration of magnesium stores in deficient patients is simple, tolerable, inexpensive and can be clinically beneficial.
...After several weeks of strenuous physical activity, serum magnesium can increase with no change in erythrocyte magnesium levels despite a reduction in mononuclear cell magnesium levels. The authors of a study concluded that the reduction in mononuclear cell magnesium content ‘reflects a reduction in exchangeable magnesium body stores, and the onset of a magnesium deficiency state’. This study also indicates that just 6–12 weeks of strenuous physical activity can lead to magnesium deficiency. Another study concluded: ‘Serum and urinary magnesium concentrations decrease during endurance running, consistent with the possibility of magnesium deficiency. This may be related to increased demand in skeletal muscle’.
The article continues with an eye-opening discussion of dietary factors affecting magnesium status.
Dietary factors affecting magnesium status
‘Although magnesium intakes have been gradually falling since the beginning of the century, there were sharply increased intakes of nutrients that increased its requirements [particularly high vitamin D and phosphorus intakes]...The major source of phosphorus derives from soft drinks that contain phosphoric acid, the consumption of which has been rising markedly in the last quarter of a century’.
...Since 1940 there has been a tremendous decline in the micronutrient density of foods... in the UK for example, there has been loss of magnesium in beef (−4 to −8%), bacon (−18%), chicken (−4%), cheddar cheese (−38%), parmesan cheese (−70%), whole milk (−21%) and vege- tables (−24%).61 The loss of magnesium during food refining/processing is significant: white flour (−82%), polished rice (−83%), starch (−97%) and white sugar (−99%).12 Since 1968 the magnesium content in wheat has dropped almost 20%, which may be due to acidic soil, yield dilution and unbalanced crop fertilisation
Magnesium deficiency in plants is becoming an increasingly severe problem with the development of industry and agricul ture and the increase in human population’.Processed foods, fat, refined flour and sugars are all devoid of magnesium, and thus our Western diet predisposes us to magnesium deficiency.
... Increased calcium and phosphorus intake also increases magnesium requirements and may worsen or precipitate magnesium deficiency... The American diet is low in calcium and fiber as well as in magnesium, and high in protein and phosphorus’. Excess calcium, phosphorus and vitamin D may also lead to increased magnesium loss increasing magnesium requirements.
...patients with diabetes appear to be magnesium-deficient and magnesium deficiency likely increases the risk of diabetes.
Dietary aluminium may lead to magnesium deficit by reducing the absorption of magnesium by approximately fivefold, reducing magnesium retention by 41% and causing a reduction of magnesium in the bone. And since aluminium is widely prevalent in modern-day society (such as in aluminium cookware, deodorants, over-the-counter and prescription medications, baking powder, baked goods, and others), this could be a major contributor to magnesium deficiency.
A common misconception is that consuming phytate-rich foods can lead to nutrient deficiencies particularly magnesium depletion via binding by phytic acid. However, urinary magnesium excretion will drop to compensate for a reduction in bioavailable magnesium. And most high-phytate foods are also good sources of magnesium (grains and beans are good examples). Thus, it is unlikely that consuming foods high in phytate will lead to magnesium depletion. However, a vitamin B6-deficient diet can lead to a negative magnesium balance via increased magnesium excretion.
Supplementing with calcium can lead to magnesium deficiency due to competitive inhibition for absorption, and oversupplementing with vitamin D may lead to magnesium deficiency via excessive calcium absorption and hence increase the risk of arterial calcifications. Use of diuretics and other medications can also lead to magnesium deficiency.
Diagnosing magnesium deficiency is tricky, with long-term damage from deficiency. That’s why magnesium supplementation makes for a huge public health solution at very low cost— supplement and forget about the tests, which might be wrong anyway!
‘The existence of subacute or chronic magnesium defi- ciency is difficult to diagnose. Because the tissues damaged by magnesium depletion are those of the cardiovascular, renal and the neuromuscular systems, early damage is not readily detectable. It is postulated that long-term suboptimal intakes of magnesium may participate in the pathogenesis of chronic diseases of these systems’.
Magnesium deficiency is extremely hard to diagnose since symptoms are generally non-specific, there are numerous contributing factors, and there is no simple easy way to diagnose magnesium deficiency....
...This study suggests that a significant subclinical magnesium deficit, not detected by serum magnesium, was present in many of these healthy elderly subjects. Magnesium supplementation improved magnesium status and renal function’.
Consequences of magnesium deficiency can be severe.
Hypertension ‘Magnesium status has a direct effect upon the relaxa- tion capability of vascular smooth muscle cells and the regulation of the cellular placement of other cations important to blood pressure - cellular sodium:potassium (Na:K) ratio and intracellular calcium (iCa(2+)). As a result, nutritional magnesium has both direct and indirect impacts on the regulation of blood pressure and therefore on the occurrence of hypertension’.
Many patients with hypertension are treated with thiazide and loop diuretics, both of which deplete the body of magnesium, and giving patients with hypertension who are receiving long-term thiazide diuretics oral magnesium supplementation significantly reduces blood pressure. In fact, the high intracellular calcium induced by magnesium deficiency may induce both insulin resistance and hypertension.
...Low magnesium levels can promote endothelial cell dysfunction, potentially increasing the risk of thrombosis and atherosclerosis. Magnesium deficiency also promotes a proatherogenic phenotype in endothelial cells. Hypomagnesaemia can impair the release of nitric oxide from the coronary endothelium, while magnesium therapy can improve endothelium-dependent vasodilation in patients with coronary artery disease.
...this makes magnesium supplementation a promising therapy in the treatment of hypertension and coronary artery disease.
Atherosclerosis
With my awful CT heart calcium score, atherosclerosis of my LAD is of keen concern to me. I want to at least halt the progression, if not reverse it lest I succumb as per my internist to a “heart attack within 7 years”.
My doctors wanted to give me a statin (poison). Why did they not even mention magnesium which should lower LDC and increase HDL?
Magnesium deficiency and magnesium depletion in soft tissues can cause calcifications in the heart, liver and skeletal muscles... magnesium deficiency damages the kidneys due to calcium deposits and may cause numerous electrolyte abnormalities... supplementing with magnesium has been found to improve endothelial function in patients with coronary artery disease.
... eating a diet deficient in magnesium predisposes to atherosclerosis, calcification of the aorta, degeneration of myocardial muscle fibres and inflammatory connective tissue throughout the body...
Magnesium treatment for 3 months in patients with ischaemic heart disease increases the apolipoprotein A1:apolipoprotein B ratio by 13%, decreases the apolipoprotein B concentrations by 15%, and decreases very- low-density lipoprotein concentrations by 27%. Magnesium therapy also tended to increase high-density lipoprotein. The authors of the study concluded: ‘...magnesium deficiency might be involved in the pathogenesis of ischemic heart disease by altering the blood lipid composition in a way that disposes to atherosclerosis’.
In hypomagnesaemic kidney transplant recipients, magnesium supplementation significantly decreases total cholesterol, low-density lipoprotein and total cholesterol:high density lipoprotein ratio. Magnesium deficiency may enhance vascular endothelial injury, promoting the development and progression of atherosclerosis.
Magnesium deficiency may supersaturate bodily fluids with octacalcium phosphate calcifying soft tissues, whereas magnesium therapy may stop or even prevent soft tissue calcifications...magnesium deficiency predisposes to lipoprotein peroxidation and atherosclerosis...‘We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the serum magnesium would lead one to suspect, and may contribute to clinical cardiovascular morbidity’
Considering that around 25% of all myocardial infarctions are not due to atherosclerotic plaque rupture, coronary artery spasm induced by magnesium deficiency may explain some of these events.
...Another study in postmenopausal women found that a low-magnesium diet (approximately 100 mg/day) can induce atrial fibrillation and increases glucose levels... dietary intake of magnesium or low magnesium levels can predispose to arrhythmias. Diuretics and digoxin also cause magnesium depletion, making the heart more susceptible to the development of arrhythmias.
...meta-analysis of 19 randomised trials using magnesium orotate found a significant reduction in first-degree mitral valve prolapse, grade 1 regurgitation, supraventricular and ventricular premature contraction, and paroxysmal supraventricular tachycardia.
‘...low heart muscle magnesium may contribute to sudden death after myocardial infarction... Increasing the magnesium content of the diet may help to prevent ischemic heart disease, and there is already evidence that magnesium salts can have beneficial effects on established heart disease’.
...patients who have lower than normal magnesium concentrations in their heart muscle may be more likely to die suddenly after a myocardial infarction.
Administration of magnesium salts has been shown to reverse many of the changes in animal models of heart disease...There is also good evidence from some animal studies that pretreatment with magnesium salts protects against many of the changes in the heart caused by anoxia...’ In other words, consuming a diet high in magnesium may prevent the harms from an acute ischaemic events.
...Just 42–64 days on a diet low in magnesium (~101 mg/day) produced atrial fibrillation and flutter in three of five postmenopausal women (ages 47–75 years). Moreover, the arrhythmias responded quickly to magnesium supplementation.
In a randomised, double-blind, placebo controlled study on 350 patients with acute myocardial infarction, intravenous magnesium sulfate given immediately after completion of thrombolytic therapy significantly reduced all-cause mortality (3.5% vs 9.9%, P<0.01) and ventricular arrhythmias.
...Thus, magnesium may prevent thrombotic events and may also protect cardiac cells against ischaemia... All of these suggest that magnesium is an anti- thrombotic and antiplatelet agent and that magnesium deficiency may promote thrombosis. Furthermore, magnesium deficiency appears to be more prevalent heart disease, suggesting a need for magnesium treatment.
Conclusion
Smart move: it would be wise for everyone to supplement with a baseline amount of magnesium, for a major positive impact on world health.
Subclinical magnesium deficiency is a common and 19. under-recognised problem throughout the world. Importantly, subclinical magnesium deficiency does not mani fest as clinically apparent symptoms and thus is not easily recognised by the clinician.
Despite this fact, subclinical magnesium deficiency likely leads to hypertension, arrhythmias, arterial calcifications, atherosclerosis, heart failure and an increased risk for thrombosis. This suggests that subclinical magnesium deficiency is a principal, yet under-recognised, driver of cardiovascular disease.
A greater public health effort is needed to inform both the patient and clinician about the prevalence, harms and diagnosis of subclinical magnesium deficiency.
Which magnesium?
See Health and Vitality Start with getting Key Nutrients.
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