Lead poisoning and the gout connection

Recently, gout has inundated the business and health news. The big stories are about US Federal Drug Administration’s approvals of new uric acid lowering drugs for gout and hyperuricemia. Scientists at John Hopkins University also made the news claiming to have found the “gout gene.”

Population studies indicate that there is an alarming worldwide increase of gout, and the pharmaceutical companies see a potential billion-dollar a year market in developing new uric acid lowering drugs. The rising tide of gout suffers has also sparked new interest among financially stressed universities as a means to obtain lucrative research grants.

Uric acid is a product of the liver and is essential to many metabolic functions, such as regulating protein synthesis, forming the DNA, and regulating body temperature as well as functioning as a metabolic antioxidant and eliminating wastes from the body.

When kidney function is somehow impaired and does not eliminate uric acid properly, the result is a buildup in the blood (hyperuricemia). In some people that causes painful gout.

Today, most gout research is predicated on archaic notions and misinformation about the causes of gout. Consequently, many gout drugs simply alleviate a symptom and mask potentially fatal health problems.

The foremost misconception is that the primary cause of gout is overindulgence of rich foods and alcohol consumption. This misconception takes its roots from face value accounts of the indulgent lifestyles associated with gout suffers of historical significance.

Many researchers use that erroneous assumption as a factual foundation for scientific research into formulating new drug treatments for gout. However, throughout history there is an inextricable link between lead poisoning and gout (saturnine gout) among the aristocracy and affluent. Most researchers and medical professionals either ignore or are ignorant of the historic lead poisoning/gout connection. 

The cause of gout among the celebrities of ‘olde’ wasn’t so much about what they ate and drank, but more related to the lead content of what they ate from, what foods and drink were stored in, lead acetate sweetening agents, use of lead based cosmetics, paints and pigments, and even the use of lead salts in the medicines.

The prominent figures in history always put forth as examples of gout suffers were almost certainly afflicted with lead poisoning that caused their gout.

Lead poisoning promotes kidney damage and inhibits uric acid excretion causing it to buildup in the blood (hyperuricemia). Hyperuricemia is the most common cause of gout, and toxicologists view gout as a primary symptom of lead poisoning.

Benjamin Franklin is an example of a famous person often cited in gout articles mainly because he was a rotund individual known for his enjoyment of the good life, and perceived overindulgent lifestyle.

In Franklin’s day, lead poisoning was of epidemic proportions on both sides of the Atlantic. During his lifetime, there was extensive use of lead products to make food storage containers, glass, and glazes for pottery. Lead acetate was a primary sweetener for bread, desserts, wines, and food. They painted their homes with lead based paints, and it was in the distilled spirits and fortified wines they drank as well as the containers in which they were stored. They added lead to tobacco snuff and even to black pepper. Hair and bone analysis of exhumed skeletal human remains from the American Colonial Period commonly show high levels of lead.

In the 18th - 19th centuries, there was also gout epidemic in Britain attributed to the consumption of lead acetate laced fortified wines and cider made by lead presses (Devon Colic). It was also commonplace for the affluent gentry and aristocracy of that period to have a bowl of lead acetate sitting on the dinner table for those who desired added sweetness to their food or drink.

Gout was also rampant among the patricians and plebeians of the Roman Empire, as was lead poisoning. Historians view lead poisoning as a primary factor in the fall of the Roman Empire. The documented relationship between lead poisoning and gout dates back to the early Egyptians. Analysis showed high lead levels in the mummies’ hair and there was also documentation of gout among the royalty.

Down through 6000 years of documented history, the association between lead poisoning and gout with historical figures is unequivocal.

In the modern annals of toxicology and history of lead poisoning, the gout of ‘olde’ is always attributed to lead poisoning, not the overindulgence of protein rich foods and alcohol as most medical professionals state as fact.

Today, the increasing incidence of gout in populations and the time-line for developing gout symptoms can once again be associated with lead poisoning. This is due to the extensive use of leaded petrol, lead-based paint, and industrial pollution in the post World War II era.

People born between 1945 and 1971 stand the greatest chances of developing gout and hyperuricemia as symptoms of lead poisoning. Aside from all other exposures to lead, the most ubiquitous during that period was from the use of leaded petrol.

From the onset of adding lead to petrol, many scientists foresaw the potential of mass subclinical lead poisoning among populations.

In 1924, Yandell Anderson, professor of applied physiology at Yale University, the inventor of the gas mask, was among those who warned about mass poisoning from leaded petrol.

In 1965 that Clair Patterson, a geochemist, proved that lead in human bodies had increased 100 times since the introduction of lead in petrol.

In 1980, the US National Academy of Sciences said that leaded petrol was the greatest source of atmospheric lead pollution.

Leaded petrol was most likely the worst culprit aside from lead-based paints and lead plumbing in homes for lead poisoning. Not only did the lead from petrol pollute the air, soil, and water, but also the food crops used to feed people and farm animals. Lead pollution from petrol became a part of the food chain, and was in everything we consumed.

The most insidious aspect of the pollution from leaded petrol is that it can readily be absorbed through the skin and directly into the blood stream. The pollution also has the mischievous distinction of being readily available via all routes of exposure: oral, inhalation, and absorption through the skin.

With the phasing out of leaded petrol in the United States, the blood lead levels of all Americans declined 78 percent between 1978 and 1991. The decline was in exact proportion to the declining levels of lead in the petrol supply and coincided with the reduction of lead air pollution. The results were similar in countries around the world that phased out the use of leaded petrol for on-road vehicles.

However, just because there was dramatic reduction of environmental pollution from leaded petrol, the health problems associated with long-term exposure were not. The adverse health effects of lead poisoning are not always immediate and often manifest themselves decades later in the form of hypertension, cardiovascular disease, presenile dementia, impaired cognitive ability, and kidney damage, among others, including gout.

95% of all lead to which we are exposed is stored in the bone, and has a half-life of 28 years.

Lead is what toxicologists refer to as a “bone seeker.” It acts like calcium and becomes part of the bone structure. Consequently, our bones are a lead repository, and due to low-level, environmental lead exposures over a period of years, the lead content can reach toxic levels.

Recently, researchers found convincing evidence that many gout cases may well be associated with reabsorption into the blood of ambient lead stored in our bones.

The reason for their conclusions is that a process called bone remodeling becomes more active in middle-aged people and increases with ageing.

Bone remodeling occurs when the bone releases calcium part of the natural calcium turnover in the body. The metabolic process also releases the stored lead that causes kidney damage which in turn inhibits uric acid excretion. There is a subsequent buildup of uric acid in the blood (hyperuricemia) that causes gout in some people.

According to some research, lead reabsorption from bone remodeling may be a primary cause of hyperuricemia and gout among middle aged and elderly men, as well as postmenopausal women.

The result of reabsorbed bone-lead is lead poisoning in people not otherwise exposed to occupational levels during their lifetime. In U.S. population surveys, the results showed that second only to young children, older adults have among the highest blood lead levels from non-occupational exposures.

While exposures to the average person may be below occupational levels, over time these little exposures can add up to toxic levels in the bones. The actual impact of subchronic lead poisoning on an individual’s health does not manifest until bone remodeling begins to increase with age and larger amounts of stored lead enter the blood stream.

Reliance on the results of simple blood tests for lead levels is a poor indicator of the total body burden, and only reflects recent exposures. X-ray fluorescence is the standard for accurate determination of the total body burden.

Because of the unequivocal, historic association between lead poisoning and gout and the more recent reality of population scale exposure to lead pollution from leaded petrol, subclinical lead poisoning should be the first thing a doctor considers as the primary cause of gout.

Prescribing uric acid lowering drugs will do little more that mask the problem. If a patient is suffering from lead poisoning, at the end of the day, the doctor may lower the uric acid levels, temporarily relieving the gout attacks with drugs. However, the patent is still suffering from the deleterious effects of lead poisoning and the kidneys continue deteriorating – the doctor has only treated a symptom, not the cause.

When it comes to treatment, toxicologists should address lead related gout intervention, not medical doctors. A toxicologist would most likely recommend chelation therapy and therapeutic doses of vitamin C. Therapeutic dosages of vitamin C and potassium acetate/citrate also facilitate the excretion of uric acid without further damaging the kidneys with uric acid lowering drugs that only address the symptom.

###