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A higher white blood cell count may be an important predictor for cardiovascular disease incidence and mortality, cancer mortality, all-cause mortality, decline in lung function; so, an important predictor for heart attacks, strokes, declining lung function, dying from cancer, and premature death in general. No surprise, as the number of white blood cells we have circulating in our bloodstream is a “marker of systemic inflammation.” Our body produces more white blood cells day to day in response to inflammatory insults.
We’ve known about this link between higher white counts and heart attacks since the 70s, when we found that higher heart attack risk was associated with higher white blood cell counts, just like it was with higher cholesterol levels and higher blood pressures—something that’s been found in nearly every study done since then. Decades of studies, involving hundreds of thousands of patients, showing “dramatically higher…mortality rates” in those with higher white counts.
But why? “Why does…white blood cell count predict mortality?” Maybe because it’s a marker of inflammation and oxidation in our body. In fact, maybe even a biomarker for how fast we’re aging. But, it may be more than just an indicator of inflammation, but an active player, contributing “directly” to disease via a variety of mechanisms, including the actual “obstruction” of blood flow.
The average diameter of white blood cells is like seven and a half micrometers, whereas our tiniest vessels are only like five micrometers wide. So, the white blood cell has to squish down into like a sausage shape to squeeze through. And, when there’s inflammation present, these cells can get sticky. Here’s more images of a white blood cell plugging up a vessel as it exits a small artery, trying to squeeze into a capillary—slowing down or even momentarily stopping blood flow. And, if it gets stuck there, it can end up releasing all its internal “weaponry,” normally reserved for “microbial invaders,” and damage our blood vessels. This may be why in the days leading up to a stroke or heart attack, you may find a spike in the white cell count.
Whether white count is just a marker of inflammation, or an active participant, it’s better to be on the low side. How can we reduce the level of inflammation in our body? Staying away from even secondhand smoke can help drop your white count about half of a point. Those that exercise also appear to have an advantage, but you don’t know if it’s cause and effect unless you put it to the test. Two months of Zumba classes—just one or two hours a week—led to about a point-and-a-half drop in white count. In fact, maybe that’s one of the reasons exercise is so “protective.” But is that just because they lost weight?
“Fitness and fatness” appear to both play a role. More than half—51.5%—of obese persons with low fitness have white counts above 6.6. But those who are more fit, or who have less fat, are less likely to be up that high. Of course, that could just be because exercisers and leaner individuals are eating healthier, eating less inflammatory diets.
How do we know excess body fat itself increases inflammation, increases the white count? You’d have to find some way to get people to lose weight without changing their diet or exercise. How’s that possible? Liposuction! If you suck about a quart of fat out of people, you can significantly drop their white count by about a point. So, maybe this should get us to rethink the so-called normal reference range for white blood cell count. Maybe we should revise it downward, like we’ve done for cholesterol and triglycerides.
Up until now, we’ve just based normal values on people that might be harboring significant background inflammatory disease. If you just restrict it to those with normal C-reactive protein, another indicator of inflammation, then instead of normal being 4.5 to 10, maybe we should instead revise it closer to 3 to 9.
Okay, but where did the healthiest populations fall—those not suffering from the ravages of chronic inflammatory diseases, like heart disease and common cancers? Populations eating diets centered around whole plant foods average about 5, whereas in the U.S., at the time, it was closer to 7 or 8. The reason we know it’s not genetic is if you take those living on traditional rural African diets, who are down around 4 or 5, and move them to Britain, they end up closer to 6, 7, or 8. Ironically, the researchers thought this was a good thing—referring to the lower white counts on the uncivilized diet as neutropenic, meaning too few white blood cells. They noted that during an infection or pregnancy, where you really do need more white cells, the white count came right up to wherever necessary. So, bone marrow of those eating traditional plant-based diets had the capacity to create as many white cells as needed but “suffers from understimulation.” They’re just not smoking enough cigarettes and eating as many inflammatory foods.
Similar findings were reported in Western plant-eaters, with an apparently stepwise drop in white count as diets got more and more plant-based. But maybe there are non-dietary factors, such as lower smoking rates, in those eating healthier? What you need are interventional trials to put it to the test. Just 21 days of removing meat, eggs, dairy, alcohol, and junk affected a significant drop in white count, even in people who started out down at 5.7.
Those that started out even higher—patients with rheumatoid arthritis starting up around 7? No change in the control group that didn’t change their diet, but a one-and-a-half point drop within one month on whole food, plant-based nutrition. That’s a 20% drop. That’s more than the drop in inflammation one might get quitting a 28-year pack-a-day smoking habit.
The most extraordinary drop I’ve seen was in a study of 35 asthmatics. After four months of a whole food, plant-based diet, their average white count dropped nearly 60%, from up around 12 down to 5, though there was no control group, and not enough patients to achieve statistical significance.
If white blood cell count is such a clear predictor of mortality, so inexpensive, and reliable, and available, why isn’t it used more often for diagnosis and prognosis? Maybe it’s a little too inexpensive. The industry seems more interested in fancy new risk factors you can bill for.