So this morning I went for a run with a fellow who had surgery for really bad varicose veins. He disclosed this in a conversation where I suggested that he was training too hard (he said his zone 2 HR was 140-160, based on a max HR of 220: the old, debunked formula). Needless to say, he was struggling. I used to follow the same approach, so I know what it feels like.
I suggested he'd benefit from reading Maffetone's work, and he said he'd knew of Maffetone, but was following his doctor's advice. He seemed very dismissive.
Oh Lord, please help all those who follow their doctor's advice. No one else can.
So I got curious about causation of varicose veins. They're highly correlated with generic cardio-vascular disease, after all, and might well share the same cause, as the symptoms are superficially similar.
It's become overwhelmingly clear to me that oxidative linoleic acid metabolites (OxLAMs), which are produced in the body in the mitochondria, and are often highly toxic, are the likely cause.
"HODEs are stable oxidation products of linoleic acid (LA; C18:2, omega-6). LA is the most abundant fatty acid in atherosclerotic plaques, being seven times more abundant than arachidonic acid (AA). Oxidized lipids accumulate at sites of tissue injury, including atherosclerotic plaque. It was recognized more than 50 years ago that oxidized fatty acids accumulated in low-density lipoprotein (LDL) with age, particularly in individuals susceptible to atherosclerosis [Jira et al. 1998]. HODEs were 20 times more abundant in the LDL of patients with atherosclerosis compared with controls [Jira et al. 1998]. The structure of 9-HODE and 13-HODE, are shown in Figure 1, along with LA and the omega-3 fatty acid α-linolenic acid (ALA; C18:3, omega-3). Although the structures of these fatty acids differ only subtly, there is accumulating evidence that HODEs have distinct biological properties. Accumulation of HODEs in human atherosclerotic lesions was described nearly two decades ago [Kuhn et al. 1992], when they were shown to be components of both the cholesterol ester and phospholipid fractions. LA accounts for 40–45% of the polyunsaturated fatty acid (PUFA) in plaque, and 30% of PUFAs in plaque are oxidized. HODEs are the most abundant oxidation products in plaque, and they are present in all advanced lesions, although the quantity varies from patient to patient [Waddington et al. 2003, 2001]."
I've not found a randomly-controlled study just yet, (although this one comes close):
"The Lyon diet-heart study was one of the most successful intervention trials of all time. The experimental group increased their intake of fish, poultry, root vegetables, green vegetables, bread and fruit, while decreasing intake of red meat and dairy fat. A key difference between this study and other intervention trials is that participants were encouraged to eat a margarine rich in omega-3 ALA. In sum, participants decreased their total PUFA intake, decreased omega-6 intake and increased intake of ALA and long-chain omega-3s. After an average of 27 months, total mortality was 70% lower in the intervention group than in the control group eating the typical diet!"
Linoleic acid (LA) is the primary polyunsaturated omega-6 fat in the Modern American Diet. OxLAMs are produced in the body from excess LA in the diet, can be reduced by a reduction of LA from the diet, and such reduction appears to have (in one small study) a 100% success rate in reducing at least one major aspect of the Metabolic Syndrome, the primary health scourge of our time.
Took a while, a couple of hours, but here we are:
backup link here.)
I'll snip a few relevant points:
"Despite numerous theories, the etiology and pathogenesis of primary varicose veins remain unclear. The etiology of chronic venous diseases (CVDs) known as chronic venous insufficiency (CVI) is related to leukocyte trapping. Leukocyte trapping involves trapping of white cells in vessel walls followed by their activation and translocation outside the vessel. Release of reactive oxygen species (ROS) from trapped white cells has been documented. Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). The aim of this study was to determine the involvement of free radicals in the etiology of venous changes."
Well there we go. MDA, along with 4-HNE and acrolein (and a whole host of others) are OxLAMs. I will object to their statement that OxLAMs are generated by ROS, as it's clear that they're generated independently.
"The levels of oxidative stress markers strongly correlated with lesions observed by USG in insufficient and varicose veins. In both a higher concentration of MDA was observed, which is a sign of lipid peroxidation. Antioxidative mechanisms, SOD activity and total antioxidative power expressed as FRAP were inversely proportional to MDA concentration. In insufficient and varicose veins both FRAP and SOD activities were significantly lower than in normal veins. The severity of clinical changes was inversely dependent on the efficiency of scavenging of ROS, which additionally proves the participation of free radicals in pathogenesis of CVDs."
There you have it.
"These results confirm that a patients suffering from chronic venous insufficiency are constantly under oxidative stress. Their TAS is lowered and lipid peroxidation level (measured as MDA concentration) increased....
"...Interaction between leukocytes and endothelium (which results in toxic metabolites e.g., MDA; Rojas & Phillips, 1999) is promoted by slow venous flow (Danielsson et al., 2003). Mahmound et al. (2002) found strong lipid peroxidation (increased MDA concentration) around insufficient venous valves (compared to normal noninflamed vessels). This phenomenon was also confirmed in our research. Also Tryankina et al. (2003) drew attention to decreased amount of plasma antioxidants and increased lipid peroxidation in patients with varicose veins in comparison to healthy individuals. All this shows how strongly oxidative stress can decrease defense mechanisms of patients witch [sic] CVI (Wlaschek et al., 2005)."
This also suggests that the mechanism behind varicose veins is identical to that behind atherosclerosis.
LA isn't directly toxic, but it turns into poison in the body. Excess LA consumption is to be avoided like the plague.
P.S. Well, I missed this:
"First, all parameters we researched: antioxidant enzyme activity, TAS and FRAP bring us to a conclusion that the main reason behind CVI is antioxidative system dysfunction."
That's wrong. It's antioxidative system overload. Reduce the load, resolve the disease.
"Also simple modification of the patients diet and lifestyle can have beneficial effects."
They're right about that, but they don't specify what to do. If you're dealing with an overload of oxidative linoleic acid metabolites, and linoleic acid solely enters the body through the diet, the answer should be clear...