maybe you’ve heard of alzheimer’s other name; type iii diabetes?

ALZHEIMER’S OR TYPE III DIABETES?
NO REASON TO HAVE TO CHOOSE; THEY’RE THE SAME!

Is Diabetes a Form of Accelerated Aging?  A rhetorical question asked via the title of a study published in a 1976 issue of Geriatrics.

What were you doing back in 2005, and why do I ask?  It’s the first time I remember hearing about Type III Diabetes (T3D).  And while there are probably other instances that can be found earlier, understand that the term was not coined in a vacuum.  In other words, as you can see from the title above, decades of studies led to that “Ahha Moment,” where the light bulb came on and scientists actually realized that Alzheimer’s was largely due to blood sugar’s affects on the brain.  It’s an easy concept to understand once you realize that Alzheimer’s Disease has increased exponentially over the past century — in lock-step with sugar consumption.

That pillar of all knowledge (Wikipedia) had this to say about T3D; “Type 3 diabetes is a proposed term for Alzheimer’s disease resulting in an insulin resistance in the brain. The categorization is not embraced by the medical community, though a limited number of published reviews have forwarded putative mechanisms linking Alzheimer’s and insulin resistance.  The term has been widely applied within alternative healthcare circles.”  I would certainly be classified as one of those “Alternative” folk, but what I want to show you today is that this concept is not confined to alternative practitioners, and is increasingly being “embraced” by the mainstream.  BTW, just because something is or isn’t embraced by the medical community has little bearing on its veracity (HERE or HERE are good examples).  Be aware that all the studies I quote from are at least somewhat cherry-picked due to restraints on time and space.

  • TYPE III DIABETES IN 2005:   As far as I can tell, the study that got the ball rolling was from the February issue of the Journal of Alzheimer’s Disease (Impaired Insulin and Insulin-Like Growth Factor Expression and Signaling Mechanisms in Alzheimer’s Disease: Is This Type 3 Diabetes?).  The ten authors from the Pathology Department of a famous Ivy League medical school (Brown) concluded that “The neurodegeneration that occurs in sporadic Alzheimer’s disease is consistently associated with a number of characteristic histopathological, molecular, and biochemical abnormalities, including cell loss, abundant neurofibrillary tangles and dystrophic neurites, amyloid-beta deposits, increased activation of pro-death genes and signaling pathways, impaired energy metabolism / mitochondrial function, and evidence of chronic oxidative stress.  The accumulating evidence that reduced glucose utilization and deficient energy metabolism occur early in the course of disease, suggests a role for impaired insulin signaling in the pathogenesis of AD.   We propose the term, ‘Type 3 Diabetes’ to reflect this newly identified pathogenic mechanism of neurodegeneration.”  For the record, these authors did not equate AD with T3D, but showed how eerily similar the molecular mechanisms were.

 

  • TYPE III DIABETES IN 2006:  A year later we saw three different studies on the subject; Lancet Neurology’s Alzheimer’s Disease Could Be ‘Type 3 Diabetes,’ the Journal of Alzheimer’s Disease’s Intracerebral Streptozotocin Model of Type 3 Diabetes: Relevance to Sporadic Alzheimer’s Disease, and IOS Press’s Therapeutic Rescue of Neurodegeneration in Experimental Type 3 Diabetes: Relevance to Alzheimer’s Disease.  The first study answered the question raised in its title affirmatively.  The second study (again, from Brown) showed that “chemical depletion of insulin and IGF [insulin-like growth factors] signaling mechanisms combined with oxidative injury is sufficient to cause AD-type neurodegeneration. The STZ-injected rats did not have elevated blood glucose levels, and pancreatic architecture and insulin immunoreactivity were similar to control, yet their brains were reduced in size and exhibited neurodegeneration associated with cell loss [apoptosis], gliosis, and increased immunoreactivity.”  Just remember that immunoreactivity and “GLIOSOS” (activating the microglia) are hallmarks of AUTOIMMUNITY.   And in case you did not grasp what this last sentence was saying, re-read it until you do.  AD is happening from living the high carb lifestyle, in spite of the fact that your blood sugar levels might be “normal”.

 

  • TYPE III DIABETES IN 2007:  Writing for The Scientist in November of that year (Alzheimer’s: Type 3 Diabetes? Neurodegeneration Research Turns to Insulin for Answers) Kerry Gerns wrote, “Looking in the brains of patients diagnosed with Alzheimer’s disease found reductions in insulin, insulin-like growth factor. Type 1 diabetes is a deficiency in insulin production, and type 2 is a resistance to insulin, where there is plenty of insulin but cells don’t respond to it. Accumulated evidence suggests that insulin and insulin-like growth factor signaling is impaired in patients with Alzheimer’s disease. It looks like in Alzheimer’s disease you end up having a defect in these kinds of pathways, which are similar to the pathways for insulin-resistant diabetes.”   2007 also saw major media getting in on the act with Time’s article by Catherine Guthrie, Is Alzheimer’s a Form of Diabetes?  Answering the rhetorical question stated in the title, she wrote, “Referring to Alzheimer’s disease as ‘type 3’ diabetes is controversial, especially within the diabetes community. Alzheimer’s disease is a complication of diabetes, not a unique form of the disease, says Dr. Sue Kirkman, vice president of clinical affairs for the American Diabetes Association. ‘Nevertheless,’ she says, ‘this is primarily a semantic argument.’”  To reiterate her point about semantics, another scientist quoted in the article referred to the differences between the two diseases as “splitting hairs“.

 

  • TYPE III DIABETES IN 2008: In November of that year, the person who started it all — Brown’s Susan De la Monte — published yet another study (Alzheimer’s Disease Is Type 3 Diabetes: Evidence Reviewed), this one in the Journal of Diabetes Science and Technology.   “Alzheimer’s disease has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-β (APP-Aβ) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage.  We conclude that the term ‘type 3 diabetes’ accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both T1DM and T2DM.”  Don’t forget that T1D is autoimmune diabetes — the body attacking its own pancreas.

 

  • TYPE III DIABETES IN 2009:  In November of 09, Dr. Tina Kroner wrote an article for Alternative Medicine Review called The Relationship Between Alzheimer’s Disease and Diabetes: Type 3 Diabetes?  She concluded that, “Advanced glycation end products (AGEs) are found in higher concentration in both hyperglycemia and AD, contributing to oxidative stress and cell damage. These AGEs are known to be further modified to reactive advanced glycation end products, (RAGEs), which can generate oxidative injury.”  Not sure what OXIDATIVE STRESS or AGES are?  Click the links and get familiar as it’s very important since both destroy mitochondrial function — the foundation of life and health.  Dr. K went on to say, “Referring  to AD  as  type  3  diabetes  has  its  foundation  in  the  fact  that  the central nervous system  in  AD  is  characterized  by  a  paucity  of  insulin  and  resistance  of  the  insulin  receptors. This results in cognitive dysfunction, since insulin  is  crucial  for  neurological  signaling  processes  to  occur.  Insulin  also  participates  in  neurological  function  by  stimulating  the  expression  of  ChAT,  the  enzyme  responsible for acetylcholine synthesis; acetylcholine is in  turn a necessary neurotransmitter for cognition.

 

  • TYPE III DIABETES IN 2010:  In May of 10, two doctors of pharmacology, writing in the “neurology” section of the U.S. Pharmacist (Type 3 Diabetes: Brain Diabetes?) said, “A relationship between diabetes mellitus (DM) and dementia is undeniable, with numerous studies concluding that DM increases the risk of cognitive decline and dementia, including Alzheimer’s disease. Not only does DM increase the risk of dementia, it actually increases the rate of dementia development two- to threefold. The mechanism of this impairment is not fully understood, but it is hypothesized that hyperglycemia, insulin resistance, oxidative stress, advanced glycation end products, and inflammatory cytokines collectively lead to cognitive dysfunction.  The apparent overlap between DM and dementia has led to the suggestion that AD is not solely a neurologic disorder, but rather a neuroendocrine disorder.” Although the point of this article was the never-ending quest for new drugs (essentially new diabetes drugs), the thing you have to remember is that science has repeatedly shown that THIS CLASS OF DRUG does not work worth a flip.  Like STATINS that unarguably lower CHOLESTEROL LEVELS but don’t change endpoints, diabetes drugs lower blood sugar without really affecting morbidity or mortality either.  These are the surrogate endpoints that medicine loves to chase and track, but in reality don’t mean much if the process doesn’t help you live longer with less chronic illness (HERE).

 

  • TYPE III DIABETES IN 2011: 2011 was a big year for T3D. In April, six Italian researchers from the University of Palermo’s Department of Experimental Biomedicine and Clinical Neuroscience published a study in Rejuvenation Research called Can Alzheimer Disease Be a Form of Type 3 Diabetes?  These authors answered their own question by stating….  “Alzheimer disease and metabolic syndrome are two highly prevalent pathological conditions of Western society due to incorrect diet, lifestyle, and vascular risk factors. Recent data have suggested metabolic syndrome as an independent risk factor for AD and pre-AD syndrome. Furthermore, biological plausibility for this relationship has been framed within the ‘metabolic cognitive syndrome’ concept.”  Since the authors went on to describe several technical similarities between the two diseases, AD and diabetes CMS, I feel it is critical for my readers to understand what CARDIOMETABOLIC SYNDROME is, as it is arguably the #1 risk factor for both.  Researchers from the collective labs of Neurodegeneration and Neuroinflamation at BSHRI in Arizona, published a study in the International Journal of Alzheimer’s Disease (Is There Inflammatory Synergy in Type II Diabetes Mellitus and Alzheimer’s Disease?) that concluded, “There is strong evidence supporting inflammation as key feature in the brain of AD and in the pancreas of T2DM. A wide range of inflammatory mediators and receptors are involved in these two diseases, although complement activation is a prominent feature in AD, but not in T2DM. The presence of infiltrated lymphocytes is controversial in AD. Therefore, current research findings support the inflammation-based pathogenic mechanisms in both diseases.”  A study from Pancreas (Diabetes and Pancreatic Cancer) came to some shocking conclusions related to this subject saying that, “Long-standing diabetes increases the risk of pancreatic cancer by 40% to 100%, and recent-onset diabetes is associated with a 4- to 7-fold increase in risk, such that 1% to 2% of patients with recent-onset diabetes will develop pancreatic cancer within 3 years. Type 2 and type 1 diabetes mellitus increase the risk of pancreatic cancer with a latency period of more than 5 years. Type 3 diabetes mellitus is an effect, and therefore a harbinger, of pancreatic cancer in at least 30% of patients.”  If this doesn’t present you with a  “holy crap” moment, I’m not sure what will!

 

  • TYPE II DIABETES IN 2012:  2012 saw a barrage of media coverage on the subject, with articles in the New York Times (Is Alzheimer’s Type III Diabetes?), The Guardian (Alzheimer’s Could be the Most Catastrophic Impact of Junk Food), and Popular Science (Alzheimer’s May Be Caused By Poor Diet).  All are free online.

 

  • TYPE III DIABETES IN 2013:  In November of that year, Expert Review of Clinical Immunology finally got GUT HEALTH and MICROBIOME in on the act with a study called The Intricate Association Between Gut Microbiota and Development of Type 1, Type 2 and Type 3 Diabetes.  Not surprisingly, the European authors concluded that, “It has been proposed that changes in the composition of gut microbiota contribute to the development of diabetes Types 1, 2 and 3 (the latter known as Alzheimer’s disease). The onset of these diseases is affected by complex interactions of genetic and several environmental factors. Alterations in gut microbiota in combination with specific diets can result in increased intestinal permeability [Leaky Gut Syndrome] via a continuous state of low-grade inflammation to the development of insulin resistance. Since a change in composition of gut microbiota is also suggested to be the underlying factor for the development of obesity, it is obvious to link gut microbiota with the pathogenesis of diabetes. In addition, insulin resistance in the brain has been recently associated with Alzheimer’s disease.”  So, if you’ve got DYSBIOSIS, start figuring out what it will take to get rid of it — including possibly an FMT.  A Portuguese study published in Biochimica et Biophysica Acta (Crosstalk Between Diabetes and Brain: Glucagon-Like Peptide-1 Mimetics as a Promising Therapy Against Neurodegeneration) explained how GLUCAGON, the metabolic opposite of insulin, is “neuroprotective“.  Not sure that the whole build-a-better-drug thing worked out so well for these researchers, but you don’t need drugs to increase glucagon levels — you can do it via EXERCISING and CARB RESTRICTION.

 

  • TYPE III DIABETES IN 2014:  The journal CNS & Neurological Disorders – Drug Targets was looking for potential AD drugs with a study called Molecular Linkages Between Diabetes and Alzheimer’s Disease: Current Scenario and Future Prospects.  A study from Texas Tech (Diabetes Mellitus and Blood-Brain Barrier Dysfunction: An Overview) was published in the Journal of Pharmacovigilance showing how inflammation is not only a factor in diabetes, it’s related to T3D via something similar to LEAKY GUT SYNDROME that science is starting to call LEAKY BRAIN SYNDROME.  “Changes in plasma glucose levels (hyper- or hypoglycemia) have been associated with altered BBB transport functions (e.g., glucose, insulin, choline, amino acids, etc.), integrity (tight junction disruption), and oxidative stress in the CNS microcapillaries. Last two implicating a potential causal role for upregulation and activation of the receptor for advanced glycation end products (RAGE). This type I membrane-protein also transports amyloid-beta [plaques] from the blood into the brain across the BBB thus, establishing a link between type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (also referred to as “type 3 diabetes”). Hyperglycemia has been associated with progression of cerebral ischemia and the consequent enhancement of secondary brain injury.”  This is part of the reason BRAIN INJURIES are associated with a host of strange and seemingly unrelated problems. Biochemical Pharmacology (Brain Metabolic Dysfunction at the Core of Alzheimer’s Disease) concluded “Growing evidence supports the concept that AD is fundamentally a metabolic disease with molecular and biochemical features that correspond with diabetes mellitus and other peripheral insulin resistance disorders. Disease pathogenesis is complicated by the fact that AD can occur as a separate disease process, or arise in association with systemic insulin resistance diseases, including diabetes, obesity, and non-alcoholic fatty liver disease.”  BTW, OBESITY is the #1 cause of NAFLD.  The European Journal of Neuropsychopharmacology (Type 3 Diabetes is Sporadic Alzheimer’s Disease: Mini-Review) revealed that “Alzheimer’s disease is the most common cause of dementia in North America. Because the fundamental abnormalities in AD represent effects of brain insulin resistance and deficiency, and the molecular and biochemical consequences overlap with Type 1 and Type 2 diabetes, we suggest the term ‘Type 3 diabetes’ to account for the underlying abnormalities associated with AD-type neurodegeneration.”  

 

  • TYPE III DIABETES IN 2015:  More questing for drug therapies in 2015, with Clinical Interventions in Aging publishing Link Between Type 2 Diabetes and Alzheimer’s Disease: From Epidemiology to Mechanism and Treatment.  The Italian journal Neurological Sciences also published Linking Insulin with Alzheimer’s Disease: Emergence as Type III Diabetes.  But the best of the lot was from the World Journal of Diabetes (Molecular and Biochemical Trajectories from Diabetes to Alzheimer’s Disease: A Critical Appraisal) that concluded “Diabetes mellitus (DM), a metabolic disorder is a major orchestra influencing brain and behavioral responses via direct or indirect mechanisms. Many lines of evidence suggest that diabetic patients apparently face severe brain complications, but the story is far from being fully understood. Type 2 diabetes, an ever increasing epidemic and its chronic brain complications are implicated in the development of Alzheimer’s disease. Evidences from clinical and experimental studies suggest that insulin draws a clear trajectory from the peripheral system to the central nervous system. This review is a spot light on striking pathological, biochemical, molecular and behavioral commonalities of AD and DM. Incidence of cognitive decline in diabetic patients and diabetic symptoms in AD patients has brought the concept of brain diabetes to attention. Brain diabetes reflects insulin resistant brain state with oxidative stress, cognitive impairment, activation of various inflammatory cascade and mitochondrial vulnerability as a shared footprint of AD and DM. It has become extremely important for the investigators to understand the patho-physiology of brain complications in diabetes and put intensive pursuits for therapeutic interventions.”  Even though the quest for new drugs is on, these authors revealed that “decades of research have yielded a range of molecules with potential beneficial effects, but they are yet to meet the expectations.”  This, folks, is as good an example of the failure of “MONOTHERAPIES” as I can think of!

 

  • TYPE III DIABETES IN 2016:   Ten researchers from the International Journal of Immunopathology and Pharmacology (Curcumin Ameliorates Insulin Signalling Pathway in Brain of Alzheimer’s Disease…) showed just how good YELLOW SPICES can be for the brains of those with T3D.  “It is a well-known fact that curcumin has anti-oxidant and anti-inflammatory properties.  We believe that curcumin may be a potential therapeutic agent that can regulate the critical molecules in brain insulin signalling pathways. Furthermore, curcumin could be adopted as one of the AD treatments to improve a patient’s learning and memory ability.”  Two other studies, Alzheimer’s Disease and Diabetes: The Common Pathogenesis from one of last year’s issues of Neuropsychopharmacologica Hungarica, and Shared Links Between Type 2 Diabetes Mellitus and Alzheimer’s Disease: A Review from Diabetes & Metabolic Syndrome provided more of the same things we’ve been seeing throughout.

 

  • TYPE III DIABETES IN 2017: That same crew of researchers from Texas Tech was back for the attack with a study called Is Alzheimer’s Disease a Type 3 Diabetes? A Critical Appraisal.  Because they presented such a mountain of evidence to the affirmative, I’m not quite sure why they called this a critical appraisal.  And while there was an overwhelming number of studies on this subject this year (I found at least 5 others that I am not mentioning because hopefully you are getting the picutre), one stood out for me because it actually tied the issue to aluminum.  Just over a month ago, the Journal of Alzheimer’s Disease (Alzheimer’s Disease as the Product of a Progressive Energy Deficiency Syndrome in the Central Nervous System: The Neuroenergetic Hypothesis) made an interesting statement in the middle of a long review — revealing something that many of you have been aware of for at least three decades — that aluminum is linked to Alzheimer’s Disease.  “Metal toxicity from chronic aluminum exposure is linked with AD and is related to decreases in PKC (protein kinase C) activity.”  Why is this a big deal?  Two reasons.  Firstly, aluminum is as close to a universal adjuvant as we have (because germs don’t do it on their own, adjuvants are included in all vaccines to purposely create inflammation in order to purposely drive your immune system to bigger and badder responses — HERE), being nearly ubiquitous in the VACCINES given to both children and adults (LIKE THIS COMMON ONE).  Secondly, PKC is an incredibly important (regulatory) enzyme, and without it functioning properly, you’ve got serious — even deadly — problems.

Fortunately, my regular readers already know about the AD / T3D relationship from the article I wrote last February — ALZHEIMER’S IS DIABETES OF THE BRAIN.  And while T2D can certainly be reversed by abandoning the HIGH CARB LIFESTYLE and cutting INFLAMMATION out of your life (remember that T2D is not so much a sugar issue as it is an inflammation issue), it’s not clear from the research to what extent Alzheimer’s can be reversed, if at all, by doing the same.  This is why the fact that today’s post showed that consuming ULTRA-INFLAMMATORY SUGAR — even in the absence of what the medical community considers to be “HIGH BLOOD SUGAR” — is a huge risk factor for developing any number of chronic diseases, including ALZHEIMER’S.  The takeaway?  On this final day of 2017, purpose in your heart to make 2018 a healthier year.  A great place to start getting your BLOOD SUGAR under control?  THIS POST, of course.

Share on facebook
Facebook
Share on twitter
Twitter
Share on linkedin
LinkedIn
Share on pinterest
Pinterest
Share on reddit
Reddit

Leave a Reply

Your email address will not be published. Required fields are marked *