Is Alzheimer’s Type 3 Diabetes?

A few months back when Livewell Villages – a specialized residential center in Alzheimer’s and dementia care – invited us to talk at their annual conference on the currently topical question of whether or not Alzheimer’s Disease (AD) is Type 3 Diabetes (T3DM), I struggled to get any of the doctors in our network to agree to go and present. I wasn’t clear why at the time, but felt it was too critical a topic to decline looking into a bit further. So I said I would do it. I am not a doctor or medical professional by training, but the area of AD and Dementia research is critical to me for many reasons: personal, collective and professional. I wanted to understand more about the dietary role of disease and unmap the clutter for myself by having actual time to do the reading and research myself.

Like the big nutritional debate, a few other currently topical diseases and the big C word that plague current human health, there seems to be a hesitance from the medical profession to speak up and take a stance on these controversial topics. I wondered if by delving into such an area, I was opening yet another Achilles heel that I didn’t necessarily want to, at a time when there was so much controversy in the field. I figured, what better time than now to explore this all and do the reading for myself to get my head around things.

I take this particular research area very personally and seriously because of losing my beloved gran, Lorna Kark, to AD when I was my son’s age. I was the youngest grandchild and loved her and her perfect Christmas roses and Fenjal smells dearly.

As her short-term memory declined, mom first got angry at her for missing school lifts. Then, she forgot me first as the youngest grandchild. I went with my mom to visit her in East London and watched her decline from a vibrant articulate woman into pretty much a drooling blob over a short period of time and it affected my life forever.

Another thing that shaped my path forever was the untimely death of my morbidly obese childhood nanny who passed away at a similar time. Emily, or as I called her, Stem, was my rock. I absolutely loved her and she was my other mom. She didn’t eat what our family ate: mom bought her and our other staff that lived on the farm I grew up on their monthly staples of pap, sugar, and samp. A huge bag of each, too heavy for me to help carry. That was what she ate, she was morbidly obese and in the end, couldn’t walk up the stairs without stopping for breath.  She embodies the story of a nation really. Losing Stem and my gran to seemingly unrelated conditions at that time set my path in a direction of trying to understand the big Why’s that would later help me fill in the gaps.

Later on, I would understand why medically perhaps the diseases they suffered came from similar roots and that this story exemplifies why lifestyle diseases are not necessarily only for the poor – although they do seem to be the victims of cheaper foods and poorer quality diets in our country – there are others too with this problem.

How and why this happens has always been on my mind, as has the reality that there are still no cures, effective treatments or actual real explanations for why this happens to one brain over the other.

Remembering my beautiful, intelligent and incredible Gran Lorna Kark who we lost to Alzheimer’s in the most terrible way

My reasons for leaving the corporate, heavily funded research world to head up The Noakes Foundation and get it out and loud on the agenda for focused, well-sourced future nutritional research come from a similar personally and collectively motivated perspective. It has taken me decades to understand the biology of my own metabolic condition and to fully understand the role of insulin resistance in the many diseases that I am more likely to suffer from than someone with optimal levels of insulin in their blood. Long before medical science starts to do the research into a disease, especially a new one that is unexpected, like the current story we are seeing with obesity, diabetes and some of the newer autoimmune diseases and cancers, there are the patients, like me, trying to make sense of it all and to heal themselves.

At 21, when I was told I had PCOS and insulin resistance, I did what most would: I got a fright, was devastated to have this diagnosis – I was such a healthy person and eater! I did the research and took the steps needed to fix what I could. For me, this then meant eating low GI for over a decade, as I was told to. I put fructose in my tea instead of sugar and ate stone ground oats every day for years. It also meant becoming a vegetarian and later a vegan for a while and also giving up my career at one point and dancing for more than ten hours a day in the quest to find my slim, healthy, vibrant, and fit former self. These things all failed me miserably. I got angrier and more confused: where was the right advice and who could I believe? At one point I did the Atkins Diet and lost 8 kgs within a few weeks, but just at that time, I lost a sister to cancer and stopped, afraid, going back to vegetarianism and low fat instead.

The list of the many things I tried and still explore for this quest is massive and endless. A cursory analysis of the money I have put into this story in the form of medical bills, specialists, alternative therapists, dietitians, boot camps and endless supplements, is startling. I have spent well over a million of my hard earned Rands as a single working mom, in the last two decades.

When I was diagnosed with fatty liver disease, the Gastroenterologist told me to buy some takkies and start eating more lettuce. But at that point, I was eating the healthiest I ever had – nearly zero fat and extremely low cal – and exercising hours each day. It had not helped me much if at all it seemed.  I was a decade before the curve and mostly now, doctors do understand that NAFLD is a symptom of too high a carbohydrate diet.

How does the story of mine, my nanny Stem’s and my gran Lorna’s all tie into what AD is and what causes it, and are they connected?

The answer is revealed when we start to look at how our diets have changed in the last fifty years, coupled with if we agree to treat and consider diabetes to be the end result of long-term poorly managed Insulin Resistance (IR).  The key driver of both conditions may be rooted in the same underlying condition that has been benignly overlooked and dismissed by medicine for too long.[1]

IR is the condition that I was told I had when I was 21, but which was misunderstood by medicine until the last few years. All the many doctors I saw from 21 until I found the superb science of Prof Noakes and had my light bulb moment, all told me that I would absolutely end up with diabetes eventually and that there was no way to really avoid it.

I now know for sure that, had I been given better advice then – dietary not really medical so much – I would be absolutely fine and well now some decades later. Sadly, in the time between then and now, I wasted years on the wrong tracks of all kinds and have longer-term metabolic damage and more severe IR which is more challenging to fully reverse.

In his book Fast Food Nation[2], Eric Schlosser talks about how, in today’s world, the average child recalls Ronald McDonald quicker than it does Santa Claus. The average school lunch box in SA has up to 26 teaspoons of hidden sugars in it, depicted in the image below from The Noakes Foundation.[3]

According to the latest South African Demographic and Health Survey, almost 70% of local women are either overweight or obese. The country has the highest rates for women in Africa.[4]

Our guidelines and our diet are failing us in such a massive way that even those who are tasked with implementing ‘health’ in places like hospitals, the navy and the dieticians themselves, are clearly obese. The navy came to us asking for advice – “Our guys are not always fitting into their uniforms and the submarine passageways are getting too narrow at the moment. We have them eating low fat and running up to 11kms a day and they are just getting fatter.” They told us, with a sense of urgency.

By late last year, public health facilities were seeing over 15,000 new cases of diabetes and close to 25 000 new hypertension cases every month, according to the health department’s District Health Information System.[5]

The high sugar and carb-laden diets are driving obesity and other chronic diseases in ways that we do not yet understand the implications of, most especially the effects of this on the human brain.

When we start to dig into the real building blocks of cerebral metabolism, some interesting things pop up that start to map out the answer to the question Livewell posed to me: is AD really T3DM?

  • The human brain is particularly rich in cholesterol: around 25 percent of all body cholesterol is accounted for by the brain.
  • Growing evidence supports the concept that AD is a metabolic disease mediated by impairments in brain insulin responsiveness, glucose utilization, and energy metabolism.
  • Insulin, previously thought to be primarily involved in glucose regulation and metabolism, is now clearly understood to be a key role player in neural processing. The brain is loaded with insulin receptors and the brain itself along with some other organs like the liver, cursorily appears to be a key organ that suffers from what we call insulin resistance.
  • The traditional or mainstream model of cerebral metabolism focuses on the glucose uptake model, typically illustrated by the PET scan below that looks at this as a way to prescribe certain metabolic and vascular conditions of the brain:

This model of analyzing and predicting future brain metabolism and disease progression has one caveat that has largely been underestimated in diagnostic care and treatment as well as under-researched as a treatment for the diseases of AD and dementia which is the metabolic model of ketone usage by the body and brain. This is where the link between diabetes and AD or dementia suddenly becomes very pertinent.

If we are to say that vascular degeneration is the key driver and ‘untreatable’ aspects of the aging and deteriorating AD brain, then surely anything that prevents and treats this particular condition from occurring or slows down the degeneration is key to preventative care and also integrative treatment?

If ketones – a source of fuel the brain seems to prefer over glucose when given the choice – are readily available and are possibly better alternative fuel blocks for the brain, readily crossing the blood-brain barrier and present in a natural dietary state adopted by many and deemed safe, why is this the ketogenic diet not, like seizure and epilepsy treatment, the prescribed diet?

I started to understand the doctor’s hesitance the further I dug into this story and had a few sleepless nights of research and scanning through some academically published studies in the area. This seemed so obvious to me surely there is more being done and more exploratory work in this area?

If the brain can receive energy from ketones and glucose (and a few other things that are required for it to function) what if this could delay the disease progression or stop it before its onset, with some simple dietary measures?

 A paper by Senneff et al[6], summarized in the infographic below, highlights how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of AD.

 

 

Could it be this simple?  Could a relatively simple dietary modification, towards fewer highly processed carbohydrates and relatively more fats and cholesterol, be a likely protective measure against Alzheimer’s disease?

My inner skeptic that knows this story decided: Too good to be true. So the digging went deeper.

Another paper by Lange et al[7], summarized in the infographic below, affirms this hypothesis again:

Compared to elderly controls, individuals with senile dementia showed a decrease in regional glucose use in the posterior cingulate, temporal, parietal and prefrontal cortex and this hypo-metabolism correlated significantly with measures of cognitive functioning. Both the direct administration of ketone bodies and the use of high-fat, low-carbohydrate ketogenic diets have been shown to be efficacious in animal models of AD and clinical trials with AD patients.

There are masses of other sources of data and many studies have been done on Alzheimer’s disease. Today, as I was writing this article, I asked myself the question of what I would do if I were to see myself or a loved one with the depressing symptoms we recognized and now know too well from our journey with my dear gran. How does anyone deal with this depressing outlook with no known successful treatment other than sit on the couch and accept a slow sad death?

Today I also fell across an article in the Wall Street Journal[8] from Pfizer saying it is stopping its research into drugs for Parkinson’s and Alzheimer’s: none of them are working or proving to be effective at improving cognitive decline. Three hundred people are being laid off currently as they close down the many research areas of drug development.

One thing we have learned for sure is that drugs are not particularly helpful over the long term, especially when it comes to chronic diseases. Whilst psychiatry is a lot more nuanced and medications have profound impacts in some areas, there are others where diet is known to be more effective. In his book Grain Brain[9], Dr David Perlmutter describes the startling effect that carbohydrates play on brain chemistry and functioning and we see this too in our self-reported patients that remit a wide variety of psychiatric conditions by the adoption of a ketogenic diet.

Dr Georgia Ede is perhaps the most outspoken psychiatrist who supports ketogenic dietary adoption for a number of conditions and is outspoken about the need for much more research into this area.

“Ketogenic diets are special low-carbohydrate diets that have been used to treat epilepsy for almost 100 years and show great promise in the management of a wide variety of other brain disorders.” [10]

Alzheimer’s, in my view, appears to be similar in nature and possibly preventable in the same vein. It, like most symptoms of degenerative lifestyle conditions (and I call it a symptom here rather than a disease deliberately), needs to be treated with lifestyle measures which address diet, blood insulin levels, inflammation and the mind-body connection.

In The End of Alzheimer’s [11], Dale Bredesen MD states frankly that “High Insulin and High Glucose are the two most important risk factors for AD” (7, page 122).  He goes on to recommend that ‘It is critical to know your insulin status. Your fasting insulin level should be 4.5 or below. Your fasting glucose should be 90 or lower, and your HBA1C should be less than 5%”. (p 123). This supports our advice at The Noakes Foundation around optimal blood markers for preventative or reversal of the condition of Type 2 Diabetes.  Again here, we are looking at the same red flags and markers as warning signs for two previously disassociated conditions.

The answer is perhaps, just perhaps, beyond clinical models of drug development, startlingly simpler than we imagined. I quote a master of simplifying complexity, Greg Glassman CEO of Crossfit here: ‘Off the carbs, off the couch’.  I would go keto, which I mostly live by and do these days because of the overwhelming evidence I see daily in my job concerning the adverse effects a carb and sugar-laden diet has on the brain. I also see daily the endless self-reported reversals of many other cognitive and psychiatric conditions that are remitted by a ketogenic diet and by cutting the carbs.

So, that’s my plan for longevity if I am lucky enough to achieve it and defy lost years of eating the wrong thing for my condition and of course, the genes!

Eat low carb. Avoid all the bad fats. Exercise. Work on my mind and stress levels. Work on my inflammation levels. Dance more.

And, yes, I would dose myself up on the coconut oil! Bring it on!

About the Author:

Jayne Bullen heads up The Noakes Foundation and its various projects, Eat Better South Africa! and the Nutrition Network. She wrote her MBA thesis at the University of Leeds Business School on the problems of advocacy and marketing to children and the danger of sugars in their diet. She went on to work on pan-European projects at the ECDC and EFSA, later heading up research and insights for the Media 24 group. She chose to leave the corporate world and to focus her time on exposing the truths of the dietary lies we have been told, committing to making research better funded in the nutrition area and was profoundly impacted in her own life and personal health challenges when she found the work of Prof Noakes and his peers. She is committed to what she calls Living Research and Better Medicine. She is also a Movement Medicine teacher and a Mind-Body Medicine Professional.

About the Noakes Foundation and the Nutrition Network:

The Noakes Foundation[12] is a Public Benefit Organization founded for public benefit which aims to advance medical science’s understanding of the benefits of a low-carbohydrate healthy high fat (LCHF) diet by providing evidence-based information on optimum nutrition. The Foundation’s key goal is to change the way South Africa eats because the epidemics of obesity and type 2 diabetes are set to cripple national health care within the next 10 years. The Foundation relies purely on funding to carry out this mandate; visit our website to find out how you can help: www.thenoakesfoundation.org/donate.

The Nutrition Network[13] is an independent initiative inspired by The Noakes Foundation and is an online learning platform designed exclusively for medical practitioners and allied health workers across all disciplines, presenting the latest and most up-to-date science and research in the field of Low Carb nutrition. On completion of the course, practitioners will receive a certificate signifying their ability to prescribe LCHF to their patients.

 

Footnotes:

[1] Refer to the explanation of this concept by Prof Tim Noakes here: https://www.youtube.com/watch?v=Ef-NZtTVSMM

[2] Schlosser, E. (2002). Fast food nation: The dark side of the all-American meal. New York: HarperCollins.

[3] Infographics can be found on The Noakes Foundation website: www.thenoakesfoundation.org/news/educational-material

[4] Statistics retried from http://www.health24.com/Diet-and-nutrition/News/nejm-obesity-study-shocking-results-20170612

[5] Statistics retrieved from http://www.statssa.gov.za/?page_id=1854&PPN=P0309.3&SCH=6987

[6] Senneff, S Wainwright, G Mascitelli, L 2011. Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet. European Journal of Internal Medicine.

[7] Klaus W. Lange a, Katharina M. Lange b, Ewelina Makulska-Gertruda a, Yukiko Nakamura, Andreas Reissmann, Shigehiko Kanaya, Joachim Hauser. 2017. Ketogenic diets and Alzheimer’s disease. Food Science and Human Wellness, vol. 6, pp1-9.

[8]Article retrieved from https://www.wsj.com/articles/pfizer-ends-hunt-for-drugs-to-treat-alzheimers-and-parkinsons-1515267654

[9]Perlmutter, D & Loberg, K (2013). Grain brain : the surprising truth about wheat, carbs, and sugar–your brain’s silent killers. New York, NY : Little, Brown and Co.

[10] Quote retrieved from https://www.psychologytoday.com/blog/diagnosis-diet/201709/low-carbohydrate-diet-superior-antipsychotic-medications

[11] Bredesen, D (2017). The End of Alzheimer’s : The First Program to Prevent and Reverse Cognitive Decline. Avery Publishing Group.

[12] www.thenoakesfoundation.org

[13] www.nutrition-network.org

 

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