I spent last weekend in Illinois to perform at a comedy club in my hometown. I also visited my dad, so of course I’ve once again got Alzheimer’s on my mind (no pun intended).
The good news is that Dad was having one of his better days when Mom and I took him out to lunch. He called me by name twice and was able to participate in the conversation a bit. He spoke briefly with a friend who happened to at a nearby table and seemed to recognize him.
Amazingly, he still shows flashes of humor. A couple of times, he got that old twinkle in his eye and said something funny — on purpose. A few weeks ago, when a lifelong friend of his was visiting and complained that a hair stylist had “gone a bit short” with her haircut, Dad turned to her very bald husband and said, “Looks like that stylist went a bit short on you too, huh, Bob?” I don’t know how a mind that can’t grasp the concept of putting on shoes can still generate humor. Maybe it’s in his DNA. I told my mom I think every Irishman’s secret wish is to die five seconds after saying the funniest line of his life.
The bad news is that his better days still aren’t good. While trying to help him put his coat on after lunch, I couldn’t get him to understand that he needed to move his arm backwards, not forwards. As my mom took him back inside the nursing home, he said, “I’m tired. I probably won’t go into the office tomorrow.” I guess those walkers will have to go unsold for a day or so.
My older brother was in the audience for the Friday-night standup show, and we talked about Dad’s condition afterwards. After I recounted the lunch with Dad, my brother said, “Well, we’re screwed.” (He was slightly more colorful, but you get the idea.) I asked why he thought so.
He replied, “Grandpa Markwell [our great-grandfather] didn’t start getting senile until he was 98. For Grandma Naughton, it was in her 80s, and for Dad, it was around 70. We’re screwed.”
I don’t think so, at least not in my case. When it comes to disease, genetics may load the gun, but we can avoid pulling the trigger. I know better than to shoot myself. Dad made two big mistakes I won’t repeat: he became a bit of sugar freak after he quit smoking (and almost certainly became progressively more insulin resistant, judging by his girth), and he took Lipitor for more than twenty years. I’ve mentioned both before, but let’s take a more detailed look.
First, statins: If you want to delve into the chemistry of how statins affect brain function, you can read this article. In the meantime, here are a few highlights:
There is a clear reason why statins would promote Alzheimer’s. They cripple the liver’s ability to synthesize cholesterol, and as a consequence the level of LDL in the blood plummets. Cholesterol plays a crucial role in the brain, both in terms of enabling signal transport across the synapse and in terms of encouraging the growth of neurons through healthy development of the myelin sheath. Nonetheless, the statin industry proudly boasts that statins are effective at interfering with cholesterol production in the brain as well as in the liver.
Researchers are only recently discovering that both fat and cholesterol are severely deficient in the Alzheimer’s brain. It turns out that fat and cholesterol are both vital nutrients in the brain. The brain contains only 2% of the body’s mass, but 25% of the total cholesterol. Cholesterol is essential both in transmitting nerve signals and in fighting off infections.
High cholesterol is positively correlated with longevity in people over 85 years old, and has been shown to be associated with better memory function and reduced dementia. The converse is also true: a correlation between falling cholesterol levels and Alzheimer’s.
Put yourself on Lipitor, and we can pretty much guarantee that your cholesterol will fall. That’s the supposed benefit. But …
Yeon-Kyun Shin is an expert on the physical mechanism of cholesterol in the synapse to promote transmission of neural messages. In an interview by a Science Daily reporter, Shin said: “If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters. Neurotransmitters affect the data-processing and memory functions. In other words — how smart you are and how well you remember things.”
A second way (besides their direct impact on cholesterol) in which statins likely impact Alzheimer’s is in their indirect negative effect on the supply of fatty acids and antioxidants to the brain. It is a given that statins drastically reduce the level of LDL in the blood serum. This is their claim to fame. It is interesting, however, that they succeed in reducing not just the amount of cholesterol contained in the LDL particles, but rather the actual number of LDL particles altogether. This means that, in addition to depleting cholesterol, they reduce the available supply to the brain of both fatty acids and antixodiants, which are also carried in the LDL particles. As we’ve seen, all three of these substances are essential to proper brain functioning.
The bottom line: your body makes cholesterol for a reason. Beat down your cholesterol with a drug, and you’re messing with your biochemistry at the cellular level. Not a good idea.
Of course, plenty of people who don’t take statins develop Alzheimer’s as well. I doubt statins are a major cause of the disease. But insulin resistance could be.
As Gary Taubes explains in Good Calories, Bad Calories, since neurons in the brain ideally last for a lifetime, they may be prime candidates for the accumulation of advanced glycation end-products, or AGEs — proteins linked haphazardly with sugars. (The acronym is convenient if not intentional; AGEs literally age your tissues.) AGEs appear to be involved in the early stages of the amyloid plaques that form in the brain. That means the foods that spike your blood sugar are already causing trouble. As an article on AGEs and diabetes explains:
A lowered glucose concentration will unhook the sugars from the amino groups to which they are attached; conversely, high glucose concentrations will have the opposite effect, if persistent.
And of course, when you spike your blood sugar, your body spikes its insulin output in response. If you become insulin resistant, your insulin will be high all the time — which in turn inhibits your brain’s ability to clear away plaques. As Gary Taubes wrote:
Insulin (in a test tube) will monopolize the attention of insulin-degrading enzyme (IDE), which normally degrades and clears both amyloid proteins and insulin from around the neurons. The more insulin available in the brain, by this scenario, the less IDE is available to clean up the amyloid, which then accumulates excessively and clumps into plaques … Mice that lack the gene to produce IDE develop version of both Alzheimer’s disease and Type 2 diabetes.
Other research has shown that insulin receptors in the brain can become resistant and waste away, just as they can in the muscles and other organs. No wonder some researchers are beginning to refer to Alzheimer’s as Type 3 diabetes.
Some months ago, I mentioned the HBO series The Alzheimer’s Project. I’ve included a 21-minute clip that addresses insulin resistance below.
I found this section of the series interesting but also somewhat annoying. Dr. Craft, the expert interviewed here, makes a good case for insulin resistance causing Alzheimer’s. But of course, she’s convinced complex carbs are good and saturated fat is bad. For the gazillionth time, complex carbs are only good compared to refined carbs. They are not good in and of themselves. Eat enough of them, and you’ll still spike your blood sugar.
She also mentioned only two diets being tested for their effects on insulin: a high-sugar/high-fat diet and a low-sugar/low-fat diet. Now, the sad truth is, when you eat refined carbohydrates and fat together, it’s the worst combination of all, for all kinds of reasons. But take away the carbohydrates, and the fat isn’t a problem. As the first article I linked points out, fats are crucial for brain function. So why aren’t the researchers including a high-fat/low-sugar diet in this study? After all, ketogenic diets have been shown to prevent plaques, at least in mice. Ketones have also been shown to improve memory in humans with Alzheimer’s.
As I mentioned before, my mom is an optimistic person and she’s handling Dad’s situation well. My wife is also an optimistic person, but I don’t want her to handle a similar situation – ever. When I’m 70, she’ll only be 56. My daughter Sara will only be 25. Alana will be 23. I’m pretty sure none of them will be ready yet to deal with seeing me fade away, as we’ve seen my dad fade away.
Great-Grandpa Markwell was sharp until he was 98 and, by the way, lived to see his 101st birthday. I still remember taking a walk with him when I was an adolescent — he was in his late 80s — and struggling to keep up. I plan to follow in those footsteps, not my dad’s. That’s one of the many reasons I eat the way I do.