Guest post written by: Amy Berger
The idea of Alzheimer’s disease (AD) as “diabetes of the brain” or “type 3 diabetes” is gaining traction. Posts about it have appeared on this site, and Robb was kind enough to let me write one of my own a while back, in response to a podcast interview he did with Dr. David Perlmutter, author of the books Grain Brain and Brain Maker.
Alzheimer’s is scary. No doubt about that. It’s scary because, other than generally striking older folks, there seems to be no rhyme or reason to it. (And these days, it strikes not-so-old folks, too. No longer can they joke and call it “Old Timer’s” disease.) Costs associated with AD are in the billions of dollars, and with millions of Baby Boomers entering their golden years, these costs are only going to increase over the coming decades. But forget the financial costs. It’s bad enough that families might end up bankrupt due to medical costs and long-term care, but when you factor in the emotional, psychological, and physical tolls Alzheimer’s exacts from its afflicted individuals and maybe even more so, their caregivers, the fact that we have answers staring us in the face but no one’s talking about them, is unconscionable.
And make no mistake. Answers are staring us in the face. Doctors claim they have no idea what causes Alzheimer’s, and there’s nothing we can do about it. But is this actually true? More than a century has passed since AD was first identified as a unique condition. In all that time, and after all the research that’s been done since then, do we really not have any clue at all about what’s going wrong in an Alzheimer’s brain?
The problem: Brain cells are starving
I’m here to tell you that in fact, we do have some pretty solid ground to stand on in terms of the etiology of Alzheimer’s and its progression and pathology. The phrase “type 3 diabetes” pretty much nails it. The fundamental problem in AD is that the brain has lost the ability to metabolize glucose effectively and efficiently. The medical literature is unambiguous on this point. In the context of a diet high in carbohydrates, wherein glucose serves as the primary source of fuel for the brain, this is obviously a disaster. The biochemical cascade that follows is fairly complicated, but the end result is, brain cells responsible for retrieving memories, processing information, and controlling proper behavior, starve to death.
In the early stages of this, the brain is able to compensate, and symptoms are minor. This is known as “mild cognitive impairment” or “early-onset Alzheimer’s.” But as time progresses and the condition worsens, eventually enough neurons are damaged or destroyed that the affected individual manifests signs and symptoms of full-blown Alzheimer’s.
Just like the hyperinsulinemia and blood glucose dysregulation seen in type 2 diabetes, there are many potential causative factors behind why the brain’s ability to use glucose as fuel becomes compromised and someone ends up with type 3 diabetes. Lifelong carbohydrate abuse and resultant insulin resistance? Too much omega-6 fat coupled with a dearth of omega-3? Decades of unrelenting stress and insufficient sleep? Decades of physical inactivity? Decades of cholesterol-lowering medication and the egregiously misguided war on cholesterol? Probably yes, to all of these. And if you know anything at all about ancestral health and mimicking our natural diets & biorhythms, then you know there are ways to address each of these factors without pharmaceutical drugs and other expensive—not to mention ineffectual—interventions. And it is likely that doing so—addressing all of these factors—will stand the best chance of preventing, delaying, and possibly even reversing the course of Alzheimer’s and other forms of neurodegeneration.
The Solution: Feed them!
If the primary malfunction in the Alzheimer’s brain is that neurons are degenerating and cognitive function is being compromised because these cells are starving to death from an ability to properly use glucose, then first and foremost, we must provide these cells with an alternative fuel—one they can use. If you’re thinking “ketones,” please give yourself a hug for me! I have written before about the potential therapeutic role of very low carbohydrate (VLC) diets for AD. I tried to make it clear that I don’t think VLC diets are required for prevention of AD, but once the condition has taken hold, and particularly if it’s severe and longstanding, then it should absolutely be the first line of intervention. (I’ve written elsewhere about the use of exogenous ketone salts & esters for AD.)
Like I said in a past post about this, when someone’s brain is starving to death, that is not the time to play around and dip one’s toes in the water to test things out. That is the time for a cannonball into the deep end. Desperate times call for desperate measures, and all that jazz. Sweet potatoes, plantains, and white rice might be perfectly fine for a young, lean, active, insulin-sensitive specimen, such as might describe many people reading here on Robb’s site. But if someone is already in the throes of this terrible neurodegeneration, they’ve got to take a different tack. I’m not a “low carb zealot” by any means. But when someone’s brain has lost the ability to properly metabolize glucose, call me crazy, but that person is probably not the best candidate for liberal amounts of starch in their diet.
We’re starting to learn that cancer is a metabolic disease, and evidence indicates this is true of Alzheimer’s as well. And because AD is a metabolic condition, dietary therapy is the obvious place to start. Addressing the other potentially contributing factors—sleep, stress, exercise—is important and, in my opinion, not negotiable. But the first, most immediate step should be a very low-carb diet. The sooner those starving neurons get fed, the sooner they (might) start working again.
Contrary to what many expert neurologists and family doctors might claim, we do know what’s going wrong in the Alzheimer’s brain, and there are simple, low-cost, scientifically sound strategies to correct it. I don’t know how medical professionals can look at the etiology of Alzheimer’s as a metabolic/mitochondrial energy crisis and not think a very low-carb or ketogenic diet should be the number one, first-line intervention.
When I began my initial research into this topic, I was stunned by the plethora of information on the links between insulin, glucose, mitochondrial dysfunction, and Alzheimer’s. The connections are overwhelming, and for doctors to claim that we have no idea what’s happening in AD or what to do about it represents either an unprecedented level of ignorance, or straight-up malpractice—neither of which instills much confidence.
The truth is, we do have answers. We do have hope. There is an antidote for the fear, despair, and powerlessness families feel upon receiving an Alzheimer’s diagnosis.
And that’s why I’ve written an e-book, called The Alzheimer’s Antidote. I had to write it, because no doctors did it first. This information is out there. I don’t know why it’s not trickling down to the offices of neurologists and family doctors. These practitioners mean well, and I’m sure they genuinely believe there’s nothing we can do about Alzheimer’s. But that’s the biggest shame of all, folks: the people we count on to help us are asleep at the wheel. I think maybe neurologists are convinced that Alzheimer’s must be really complicated, because it’s so mysterious to them. But they’re missing the boat on the most obvious, low-hanging fruit. The truth is, viewed as a metabolic and mitochondrial disorder, Alzheimer’s is not mysterious at all. It’s actually pretty damn simple. You can’t look for AD research and not be hit upside the head with papers on insulin, glucose, and mitochondrial oxidative stress. There are so many, you’d have to intentionally ignore them in order to miss the connections.
Bottom line: Conventional medicine is failing Alzheimer’s patients and their caregivers. Failing worse than roasted bone marrow at a vegan potluck. It’s all well and good to recommend learning a foreign language or taking up a musical instrument in order to keep the mind active and form new neuronal synapses. But here’s what we know for sure: Alzheimer’s disease does not result from a Sudoku deficiency, and crossword puzzles aren’t medicine.
Okay, makes sense. But does it work?!
Full disclosure: I can’t guarantee that a ketogenic or LC diet will be effective for this condition. Since you can’t patent “Eat steak and cauliflower; ditch the corn flakes,” we don’t have piles upon piles of “gold standard” randomized, controlled trials proving the efficacy of a very low-carb diet and lifestyle interventions for delaying and/or reversing Alzheimer’s progression. (Not to mention, that would require one hell of a placebo!) I wish we did, because I’m confident the results would speak for themselves. (But evidence is mounting that cognitive impairment and AD are, in fact, reversible, and they have been reversed by employing some of the strategies I write about in The Alzheimer’s Antidote.)
Based on the logical understanding of AD as a metabolic disturbance involving systemic hyperinsulinemia and a loss of effective glucose metabolism in the brain, there’s no reason a very low-carb diet shouldn’t work. If you read The Alzheimer’s Antidote, I think you’ll agree. It’s like when people with rare autoimmune conditions ask Robb if a Paleo diet will help x, y, or z disease state, and his answer is, “It couldn’t hurt!” So I’ll borrow his “greasy used car salesman” pitch and say, give it a shot.
I know what you’re thinking: Great, just what the world doesn’t need: another book about Paleo-style diets, and why fat-free bran muffins and skim milk aren’t the breakfast of champions. Good thing this isn’t that book! The Alzheimer’s Antidote is not a weight loss book. It’s not a book about the potential dangers of gluten and casein, and there are no recipes for low-carb brownies and “chocolate-frosted Paleo cake pops.” Your bookshelf is probably already overflowing with those.
So what is The Alzheimer’s Antidote? It’s a unique resource, full of potentially lifesaving information. Nowhere else has someone put together all the moving pieces and translated the scientific literature into plain English that anyone looking to help themselves or their loved ones can understand. No other book tells you exactly what is compromised in the Alzheimer’s brain, and what to do about it. No other book presents everything so logically and then gives you concrete steps you can start taking now to preserve and possibly even reclaim cognitive function.
Additionally, I go to great lengths to explain why cholesterol is an absolutely integral nutrient in the dietary strategy to fight AD. If your loved ones are still terrified of egg yolks and butter, and are popping statins like they’re Mentos, they’ll come away with a very different perspective after reading the chapter on cholesterol. Aside from information on why a low-carb diet is recommended for rescuing cognitive function, the explanation of cholesterol’s role in the brain might be the most valuable part of the book. In fact, the Mayo Clinic and the U.S. FDA both acknowledge that memory loss, fuzzy thinking, and forgetfulness are side-effects of statin drugs. We have got to get away from the idea some physicians seem to have that there is no cholesterol level too low—as if lowering cholesterol were a rousing game of limbo at a party, with all the guys & gals in white coats cheerfully shouting, “How low can you go?”
If you’re interested in seeing whether this is a resource that might be helpful for you or your loved ones, you can download a free sample of The Alzheimer’s Antidote here. It includes the table of contents, so you can see the breadth of topics covered—genetic factors (what’s the deal with ApoE4?), amyloid plaques, neuron structure & function, glycation & oxidation in the brain, adverse effects of medications common among older people, and more. It’s an e-book, but don’t let that fool you. It is over 200 pages of information and guidance to help anyone—you, your parents, your siblings, your friends, your coworkers—implement a nutrition and lifestyle strategy to combat a condition against which conventional medicine has proven completely impotent.
Also, get 10% off your purchase of the ebook using code ROBB2015 at checkout.
Thanks so much to Robb and his team for giving me this space to let you know about the e-book.
P.S. If you’re interested in learning more about this, I encourage you to check out a podcast I did with Jimmy Moore a few weeks ago. (Additional notes are here.)
P.P.S. If someone in your life is living with Alzheimer’s, but otherwise seems “healthy,” please don’t think the idea of type 3 diabetes doesn’t apply because they’re lean and not diabetic. AD has little to do with obesity or elevated fasting blood glucose. Obviously, many AD patients are not obese, and many will actually have “normal” blood sugar and A1c. This doesn’t negate AD as a problem of carbohydrate intolerance and overall metabolic derangement. The reason blood glucose and A1c remain “normal” is because of sky-high levels of insulin. Chronically elevated insulin is a disaster for Alzheimer’s. In fact, chronic hyperinsulinemia is the number one largest risk factor, regardless of genotype. It is both causative and exacerbating in AD pathology. You can have AD and not be a diagnosed type 2 diabetic. You can have AD and not be obese. You can have AD and have healthy blood sugar. AD is not type 2 diabetes’ twin brother. It is its physiological cousin. They have many similar features, all relating to hyperinsulinemia/insulin resistance, and impaired ability to harness energy from carbohydrate.
About the Author: Amy Berger, MS, NTP, has a master’s degree in Human Nutrition and is a certified Nutritional Therapy Practitioner. After years spent doing “all the right things” to lose weight and maintain optimal health, but failing to experience the expected results, she began researching and discovered that much of what we currently believe about “healthy diets” is downright incorrect. Having learned the hard way, she has dedicated her career to showing others that vibrant health does not require starvation, deprivation, or living at the gym. Men and women cannot live by lettuce alone. Real people need real food! You can read her blog at http://www.tuitnutrition.com/.
This approach is easily worth a try, given that the Standard of Care offers essentially nothing.
Anyway, I don’t see gut biome as a topic in the book (unless it’s the “Support for Digestive Function” chapter), and given that it plays a huge role in T2D, I’d expect that attending to it would have benefits in AD …
… especially given the recent (post authoring) revelation about the the vagus nerve pathway in Parkinsons.
Of course, not even known when the book was written, we have the recently discovered brain lymph system. Perhaps malfunctions in that might further explain why plaques aren’t cleared. This, alas, doesn’t immediately suggest to me any additional therapies.
“This approach is easily worth a try, given that the Standard of Care offers essentially nothing.”
John Fawkes says
Great article Chris! So I get that cutting carbs is the top priority, particularly once the disease has already taken hold. Wondering what you think of these other tactics for preventing AD when you don’t have it yet:
Cycling creatine 2-4 times a year
Fish oil supplementation
Sleeping as much as humanly possible
Which of those do you think would be helpful prevention for people who are at risk of AD?
I address most of this in the book — sleep, stress reduction, and IF have their own dedicated (if small) chapters. I also talk about potentially helpful supplements, and among them, I include alpha-lipoic acid, carnitine, and n-3s. (Plus others, such as chromium, which can help with glucose tolerance.)
Bottom line: Anything that helps reduce insulin resistance & inflammation will likely be of some benefit. I do think diet should be the foundation of a strategy to protect and possibly regain healthy cognitive function, but there is most definitely a place for the other things you listed here.
Amy – This is absolutely fantastic. As someone who has a family history of AD and has followed Paleo for a few years now, I’m happy to see someone dedicating time to research the effectiveness of a VLC diet on AD and cognitive decline. Do you have any thoughts about going on a VLC keto diet for prevention IF you are an ApoE4 carrier or have a history of AD in the family?
Thanks for the kind words. I address the issue of ApoE4 in the book and in the podcast I did with Jimmy Moore. Nutshell version: ApoE4 doesn’t *cause* AD. There are plenty of E4s who don’t develop the condition, and most people who *do* have AD are *not* E4s. The single largest risk factor, regardless of genetics, is chronic hyperinsulinemia.
I absolutely think a low-carb approach is suitable for E4s. There’s some concern over the effects of large amounts of fat on the lipid biomarkers among E4s. I lowER carb diet can be used if someone’s worried about that. One that is low-carb, but possibly not quite as high in fat as s true ketogenic diet, and possibly also using less saturated fats more monounsatured. (So maybe going easy on the dairy fats.) I address this briefly at the end of this post: http://www.tuitnutrition.com/2015/06/alzheimers-ketones-kidding-3.html
Robert Lalonde says
Great post Amy! It’s hard to imagine why the brain would not be affected by insulin sensitivity any more than the rest of the body.
Christine Lehmann says
Hi Amy. Enjoyed reading your post and how Alzheimer’s Disease may be the type 3 diabetes of our time. Interesting parallels between diabetes type 2 and AD in terms of the cells inability to metabolize glucose and hyperinsulinemia. I wasn’t surprised to read that a low-carb diet, in general, would be effective.
Janie Sansaver says
I am interested in receiving more information, new developments, etc., regarding Early-onset Alzheimer’s Disease. Thank you In advance!
Janie Sansaver says
Because of my Early-Onset A.D., I cannot process large, details. If you could advise/information in a condensed version, that would be very helpful. It took me some time to figure that out.
I hope others, such as doctors and educators could be more sensitive with more complex information. Example: Chunking information into simpler forms. Obviously, cognition is now compromised, however, I would like more information regarding podcasts about this topic. I am not a technology whiz, however, I want to in advance.I Iook forward to being a success story in the future, rather than a statistic. I understand that time is ticking, and I still need to do a lot of homework. :o) Janie Sansaver
More than anything, I fear the health care vortex. I have until recently taken VERY FEW medications, believing in the body’s intelligence to heal itself. When my doctor started me on statins, I went into a tailspin. Within less than two weeks, the brain fog was so discernible that I felt surreal. I also found that by avoiding so-called “cholesterol-laden” foods, I was eating more carbs, which made me feel like a slug. I’ll have none of that! Quit the statins, told my doctor if it were my choice to have a longer life living in fog or one somewhat shorter, fully engaged, I’d choose the latter. I’m very active, and I DO NOT believe that cholesterol count is one size fits all; the more I read about the statin trials, the more convinced I became that somebody had it mostly wrong. And, any time that it seems almost half the adult population is on a drug, there would seem to be cause for concern that something is not quite right. Additionally, I have always known instinctively that cholesterol must protect brain function much as it protects other muscle function. So, it seems that those who think much of the cholesterol taboo is a crock are no longer lone wolves in the wilderness. It also seems that my own conclusion–reached several years ago–that we were probably replacing higher cholesterol count with diabetes and Alzheimer’s and that damnable health care vortex may just be correct. Bad trade!
David Jones says
I too have been diagnosed and wish to try alternative methods to heal myself if at all possible?!
David Jones says
Sounds fascinating and superbly significant!