Disseminated intravascular coagulation (DIC) is a condition that is characterized by problems due to both clotting and bleeding. The disease can develop over weeks to months (chronic DIC) or hours to days (acute DIC) and can be anywhere from mild to life-threatening. DIC is tightly associated with other underlying diseases and conditions such as sepsis, surgery and trauma, cancer, and serious complications of pregnancy and childbirth. It is a major problem in hospitals and occurs in about 1 percent of hospital admissions in the USA.
The National Institute of Health (NIH) is not alone in stating that DIC is the result of “excessive blood clotting.” It further states that “some diseases and conditions can cause clotting factors to become overactive, leading to DIC.”1 Many articles that discuss DIC go into excruciating details about the intricacies of all the clotting factors and their relationships. However, there appears to be no explanation on why the clotting factors become overactive, leaving DIC in the “mysterious disease” category.
In this article, we’re
What Happens In Normal Scurvy And DIC?
The fundamental physiological problem here is that the patient loses the ability to repair/replace connective tissue in the vascular walls because of a severe drop-off of blood vitamin C levels. In “normal” scurvy, this is because of extremely low consumption of foods containing vitamin C. In DIC, this is because of low consumption and aggressive depletion of blood vitamin C levels tied to the underlying conditions.
Once the vitamin C levels approach zero, the vascular walls become porous and start to bleed, triggering the clotting response. Because this is a systemic problem, it occurs widely, and when the clotting factors are exhausted, there is nothing the body can do to prevent further bleeding.
Pauling’s Description Of
Atherosclerotic Heart Disease As “Scurvy”
In 1992, Linus Pauling, Ph.D., made a profound statement that atherosclerotic heart disease is a variant of scurvy because it is, in essence, a vitamin C (ascorbic acid) deficiency.2
In the paper, Pauling presented a unified theory of human CVD (cardiovascular disease). He explained that the disease is the direct consequence of the inability of man to synthesize ascorbate in combination with insufficient intake of ascorbate in the modern diet. Since ascorbate deficiency is the common cause of human CVD, ascorbate supplementation is the universal treatment for this disease. The available epidemiological and clinical evidence is reasonably convincing. According to Pauling, further clinical confirmation of this theory should lead to the abolition of CVD as a cause of human mortality for the present and future generations of mankind.
The invariable morphological consequences of chronic ascorbate deficiency in the vascular wall are the loosening of the connective tissue and
Explaining DIC In Simpler Terms
The explanation we give here is an uncomplicated extension of Linus Pauling’s description of this common form of CVD. The differences boil down to timing and the body’s opportunity to generate a protective response.
In the case of CVD, vitamin C is always present but almost always in insufficient amounts. The damage/repair cycle very slowly accumulates a backlog of unrepaired damage and takes decades to become life-threatening. Because it develops so slowly, the body has a chance to deploy a secondary response. And the plaque deposits cardiologists are concerned about are actually “nature’s perfect band-aid” to prevent bleeding in the damaged arteries. Because of this secondary response, this form of scurvy seldom involves bleeding.
In normal scurvy, very little vitamin C is available for a few months. There is not enough time for a secondary response. The vascular tissue eventually becomes porous and people who die from this type of scurvy die from internal bleeding.
In chronic DIC, some amount of vitamin C
Sometimes, the bleeding is from the circulation inside the vascular walls and can form clots that end up on the interior surface of the related blood vessel. Since there is still some minimal amounts of vitamin C in the blood and the bleeding occurs on a smaller scale, the clotting factors might not become exhausted. This might be seen as a “clotting” problem rather than a “bleeding” problem.3
In acute DIC, the underlying condition is more severe. Therefore, the available vitamin C is consumed at such a fast rate that the blood levels are quickly reduced to near zero. Repairs to the vascular tissue stop completely. If the vascular tissue is already in a
Why DIC Mostly Affects The Small Vessels
DIC is the direct result of the rapid depletion of vitamin C. Therefore, the repair side of the damage/repair cycle of vascular tissue is quickly and dramatically reduced. Larger blood vessels with thicker walls will take many more problems in the damage/repair cycle to get to the point where they will bleed. However, the thinner-walled small vessels are much more prone to the shorter-term effects of DIC.
DIC is a variety of scurvy and therefore derived from the porous condition of the vascular tissue. Vascular integrity is a nutritional concern addressed by adequate intake of nutrients such as vitamin C, copper, zinc, sulfur, and rutin. This is easily attained through the use of supplements. Dietary alternatives are also available, but these are best at addressing DIC from the preventive perspective.
Hopefully, this article has turned a mystery disease for you into
|↑1, ↑3||What Is Disseminated Intravascular Coagulation?. National Heart, Lung, and Blood Institute.|
|↑2||Rath, Matthias, and Linus Pauling. “A unified theory of human cardiovascular disease leading the way to the abolition of this disease as a cause for human mortality.” J Ortho Med 7 (1992): 5-15.|