Dementia as Type 3 Diabetes: A New Understanding of Brain Health

March 21, 2024

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Over 50 million people worldwide currently live with Alzheimer’s disease and related dementias. And that figure is projected to triple in the coming decades as populations rapidly age.

Yet despite over a century of scientific study, the root causes behind progressive neuronal dysfunction eroding memory and cognition remain unclear. And robust treatments halting neuronal loss in typical late onset Alzheimer’s disease have proven frustratingly elusive.

This has prompted researchers to probe novel pathways that could unlock the neurodegenerative drivers ravaging the minds of susceptible seniors.

One theory gathering momentum recently reframes Alzheimer’s as a form of type 3 diabetes selectively attacking the brain.

But does the evidence truly support classifying the most common dementia cause as a type of diabetes?

In this comprehensive guide, learn how Alzheimer’s relates to diabetes – including risk factors, signs to watch for and lifestyle tips to ease progression of impairment based on the latest scientific insights at this intersection of both prevalent, life-shortening conditions.

dementia is now known as type 3 diabetes 1

Table of Contents

The Alarming Rise of Diabetes and Dementia

The global epidemics of type 2 diabetes and Alzheimer’s disease grew in parallel over recent decades – both fueled by aging populations and modern lifestyles.

Today over 37 million people live with diabetes just in the US, with another 96 million showing prediabetic warning signs pointing to eventual progression.

Likewise, over 6 million Americans currently suffer from Alzheimer’s dementia, a number set to triple by 2050 as booming numbers of seniors reach ages of greatest susceptibility.

Segments of the population demonstrating higher diabetes prevalence have simultaneously started exhibiting more rapid trajectories of cognitive decline in lockstep. Hispanics, African Americans and Asians embracing more processed modern diets all show elevated incidence of both memory loss and disrupted glucose metabolism.

Yet extensive evidence now links the two conditions biologically as well – uncovering shared disease pathways provoking researchers to posit Alzheimer’s as a form of type 3 diabetes isolated to the central nervous system.

Next we’ll break down the characteristic signs of both major afflictions.

7 Key Signs of Preclinical Alzheimer’s Disease

Well over a decade can pass between the first subtle biological anomalies indicating Alzheimer’s disease is underway in the aging brain and outward disabling dementia taking hold.

This extended preclinical phase offers a critical window for intervention and prevention before destruction of too many vulnerable neurons progresses past the point of no return.

Here are 7 common indicators associated with the earliest subtle changes enroute to Alzheimer’s dementia:

Subjective Cognitive Decline

  • Self-reported worsening of recall capacity, mental clarity and quickness points to very early aberrations like amyloid plaques accumulating between neurons.

Mild Cognitive Impairment

  • More measurable deficits in memory, attention, decision making and processing speed signify advancing damage to essential hippocampal and cortical circuits.

Apathy and Depression

  • Loss of initiative, emotional blunting, social withdrawal and sadness flags progressive neuronal dysfunction disturbing mood and drive centers.

Sense of Direction Problems

  • Getting lost routinely or confusing familiar places hints at early erosion in critical orientation networks within the brain’s memory hub.

Difficulty Finding Words

  • Frequently grasping for words and substitutions in speech highlights dysfunction spreading in language centers of the brain.

Alterations in Sleep Architecture

  • Increased nighttime awakening, daytime drowsiness and disturbed REM cycles accompanies circadian rhythm deterioration and amyloid buildup.

Anxiety Regarding Symptoms

  • Metacognitive monitoring triggers appropriate self-reported apprehension as intellectual slips become harder to ignore – motivating further medical evaluation.

Catching Alzheimer’s subtly unraveling cognition early is essential for maximizing benefit from emerging medical therapies and lifestyle measures altering trajectory.

10 Cardinal Symptoms of Type 2 Diabetes to Recognize

In contrast to the gradually emergent memory and mood changes classically heralding Alzheimer’s onset, hallmark symptoms of type 2 diabetes tend to strike more abruptly – often finally prompting previously reluctant individuals to seek medical help.

Here are the most common signs indicating insulin resistance has crossed the threshold into runaway dysfunction meeting formal diagnostic criteria for type 2 diabetes:

Extreme Thirst and Frequent Urination

  • Racing thirst signifies tissues crying out for water as blood sugars rise from failing insulin signaling dehydrating cells – while surging urine output attempts flushing out excess glucose.

Sudden Weight Loss Despite Greater Hunger

  • As the body struggles getting calories into cells it increasingly metaboloizes fat and muscle reservoirs for energy even with increased eating – causing paradoxical slenderness.

Lethargy, Brain Fog and Dizziness

  • With glucose locked out of cells, feelings of depletion sap focus while lightheadedness hints at rollercoastering blood sugars and dehydration.

Tingling Sensations or Numbness

  • Nerve irritation and injury from excess circulating blood sugar creates “glove and stocking” neuropathic sensory changes especially in the hands and feet.

Blurred Vision or Retinal Damage

  • Similarly, delicate retinal blood vessels strained by oxidative glucose stresses rupture more easily engendering spots, floaters and visual changes.

Recurrent Infections and Slow Healing

  • Spiking blood sugars weaken infection-fighting white blood cells allowing more frequent fungal, bacterial and viral breakthroughs – especially in warm creases of the body. Poor circulation and immunity also delays skin healing.

Skin Changes Including Dark Patches

  • Insulin resistance commonly manifests dark velvety skin tags and moisture-loving yeast rashes due to sugar content in sweat and sebum.

Erectile Dysfunction

  • Nerve, blood vessel and hormonal dysfunction from metabolic disarray frequently disables sexual capacity in men – an early affliction warning of advancing disease.

Labile Mood Disturbances

  • The emotional rollercoaster of urgent highs and miserable lows wreaks psychological chaos as unbalanced blood sugar levels yank hormones driving temperament.

Nagging Lack of General Wellness

  • Pervasive feelings of chronic disease burden and malnutrition escalate from the body struggling to utilize or store glucose effectively at the cellular level despite weight fluctuations.

While prediabetes signs can fly under the radar for years, the overt indicators above usually finally prompt concerned individuals to seek evaluations revealing severely insulin-resistant type 2 diabetes.

Next we’ll examine the evidence supporting connections between dementia and diabetes.

The Alzheimer’s and Diabetes Overlap

Type 2 diabetes and Alzheimer’s disease not only share surging incidence as modern lifestyle diseases of aging – statistically those struggling with one condition demonstrate substantially higher susceptibility to developing the other sooner.

For example, over a 5 year span:

  • 65% of Alzheimer’s patients exhibit signs of diabetes or abnormal glucose metabolism on testing
  • Those with diabetes show 2-5 times greater likelihood of experiencing faster cognitive decline and dementia diagnoses

This clinical pattern linking diabetes to accelerating memory dysfunction decades later suggests shared disease biology slowly degrading metabolism and cognition.

Indeed, upon autopsy classic Alzheimer’s brains show not only clumps of plaque and tangles infiltrating damaged neurons but also extensive insulin resistance marked by the following core pathologies mirroring diabetic organs:

  • Inflammation – like pancreases struggling with metabolic stress, AD brains show rampant markers of chronic inflammation from cellular debris and circulating toxins like insulin, sugars and fats that trigger overexpression of inflammatory cytokines corroding tissues over years.
  • Vascular Dysfunction – Just as smaller vessels supplying the heart and limbs narrow from plaque accumulation over time in diabetics, the microvascular channels irrigating the hippocampus essential for memory formation and retrieval become increasingly choked in Alzheimer’s compromise.
  • Insulin Resistance – In diabetes, cellular walls block insulin from enabling glucose transport and utilization for energy. Similarly in later stage Alzheimer’s disease, synaptic insulin receptors critical for memory, development and neuron nourishment display drastically reduced sensitivity to insulin presence.
  • Oxidative Stress – Where out of control blood sugars provoke cascades of damaging metabolic byproducts known as advanced glycation end products or “AGES” that inflict cellular injury, cognitive research confirms similar oxidative damage from reactive oxygen species occurs in Alzheimer’s from amyloid protein fragments and aging cell components overwhelming recycling mechanisms.
  • Mitochondrial Dysfunction – The power producing engines within cells falter from insulin resistance and excess circulating glucose levels in diabetes, restricting energy availability. Likewise in Alzheimer’s, amyloid beta and tau proteins infiltrate and disable mitochondria via increasing free radical generation combined with plunging energy output.
  • Glucose Hypometabolism – Years before overt symptoms arise, imaging scans demonstrate markedly lower uptake of glucose especially in posterior brain regions reliant on this prime energy substrate in AD susceptible patients – resembling inadequate glucose utilization similarly wracking most diabetic organs over time.
  • Cerebral Microbleeds – Analogous to mini strokes instigating small vessel rupture events in organs of longtime diabetics, cascading cycles of inflammation eat away at structural supports for delicate brain blood vessels – resulting in cerebral microhemorrhages now tracked to presage future cognitive loss.

The sum of this evidence points to Alzheimer’s representing a neuroendocrine disorder of insulin signaling, metabolic regulation and inflammation specifically attacking cognition despite weight stability – thereby earning the designation of type 3 diabetes by a growing number of experts.

Next we’ll analyze the hypothesis of Alzheimer’s as a form of diabetes affecting the brain.

dementia is now known as type 3 diabetes 2

Alzheimer’s Disease as Type 3 Diabetes – The Hypothesis

The conceptual framing of Alzheimer’s disorder as a form of type 3 diabetes manifesting in nervous system tissue first emerged in 2005 from researcher Suzanne de la Monte at Brown University.

Her hypothesis contends that Alzheimer’s essentially represents a metabolic syndrome prompting insulin resistance and neuroinflammatory processes which specifically target brain regions most susceptible to insulin-signaling dysregulation like the memory encoding hippocampus.

Just as muscle, liver and fat cells gradually block insulin from enabling glucose uptake and utilization in type 2 diabetes, de la Monte’s research points to a similar inhibition of insulin receptors on neuronal cell surfaces in Alzheimer’s.

This increasingly impedes insulin’s vital roles regulating numerous cognitive functions including:

  • Energy Production – Transporting glucose across cell membranes to fuel normal neuronal activation
  • Synaptic Plasticity – Modulating connections between neurons needed for durable learning
  • Memory Encoding – Supporting hippocampal contextual details storage
  • Amyloid Regulation – Clearing amyloid beta plaque accumulation
  • Tau Phosphorylation – Preventing pathological tau tangle formation
  • Inflammation Reduction – Blunting neurotoxic cytokine immune overactivation
  • Cerebrovascular Health – Maintaining integrity of microvessels nourishing 80 billion neurons

Just as lack of insulin starves organs of energy in diabetes despite adequate caloric intake, insulin resistance in Alzheimer’s fails to correctly stimulate key transporters needed for neurons to metabolize and utilize glucose as their chief substrate – resulting in progressive starvation of essential memory circuits.

Over the course of years, increasingly desperate neurons exhaust themselves metabolically through this chronic undernourishment cascade – ultimately resulting in exhaustion, dysfunction and mass synaptic pruning.

However, unlike the acute collapse of insulin production distinguishing type 1 diabetes, or the gradual organ exhaustion known in advanced type 2 disease, Alzheimer’s neuroendocrine failure specifically targets the hippocampus, supportive glial cells and essential memory networks – leaving other brain functions relatively spared for years.

Nonetheless, the downstream impacts of neuronal energy imbalance produces the same self-reinforcing pathological protein structures linked to diabetic microvascular scarring like amyloid plaques and neurofibrillary tau tangles.

This helps explain why corrected glucose metabolism often correlates to some cognitive benefits in Alzheimer’s clinical trials while insulin nasal sprays demonstrate transient memory improvement – the starving brain extracts relief from surging insulin. Yet lasting corrections to metabolic equilibrium proves elusive as degenerating neurons fail to fully utilize or store incoming glucose long term.

In summary, the type 3 diabetes hypothesis contends Alzheimer’s arises from brain specific insulin resistance generating gradually advancing synaptic failure rooted in metabolic deficiency and inflammation – despite ample glucose availability from normal dietary intake.

Now we’ll examine common risk factors and disease markers supporting this diabetes 3 model.

7 Key Risk Factors and Markers Supporting the Type 3 Diabetes Hypothesis

According to Dr. Suzanne de la Monte, just as markers like obesity, high cholesterol and hypertension presage diabetic diagnoses years later, she contends complex metabolic factors similarly set the stage for eventual Alzheimer’s decline by engendering insulin resistance weakening neuron integrity over time.

Here are 7 notable risk factors and disease indicators she believes point to Alzheimer’s classifiable as type 3 diabetes centered in the brain:

Elevated Fasting Blood Sugar

  • Those with higher than 100 mg/dL fasting plasma glucose ran almost 40% greater likelihood of dementia over a decade Australian study – despite technically normal glycemia.

Midlife Hyperinsulinemia

  • Having chronically excessive insulin promotes subsequent diabetes. Researchers suspect early high insulin also provokes brain insulin resistance triggering AD decades later as peripheral resistance continues climbing.

Abdominal Obesity

  • Bellies bulging with visceral fat pump out adipokines and inflammatory signals promoting insulin resistance with effects infiltrating the hypothalamus – potentially altering appetite and neurotransmitter balance to influence neurodegeneration risk over decades.

Vascular Pathology and Hypertension

  • Just as mini strokes and hypertension portend vascular dementia, they equally disturb the delicate blood vessels supplying hippocampal neurons in Alzheimer’s via inflammatory and structural injury cascades researchers believe also link with insulin resistance.

Homocysteine Elevation

  • This amino acid predicting heart disease likelihood also independently associates with poorer memory years later – potentially from enzyme impacts on insulin receptors and promoting cerebrovascular inflammation.

Elevated Triglycerides and Cholesterol Signals

  • Dyslipidemia alters insulin receptor activity through direct impacts on cell membranes. Balance requires correction to maintain transport capacity and prevent atherosclerotic effects.

Depression and Psychiatric History

  • Mood disorders show connections to neurotransmitter imbalances, cognitive function and inflammation – all potentially influenced by the brain insulin resistance cycle centered in moniker type 3 diabetes according to some psychiatry researchers.

Taken together, the majority of dementia risk modifiers indicate chronic metabolic disturbances on the periphery signaling incipient brain insulin resistance brewing with aging eventually tipping memory and neuronal integrity off the cliff.

This spectrum of shared cardiometabolic and cognitive disease markers continue forging links between diabetes and Alzheimer’s – yet direct causality remains unproven.

Skepticism and Competing Hypotheses Remain

Despite the circumstantial correlations and pathological parallels uniting Alzheimer’s with diabetes, ample skepticism remains among experts regarding several components underlying the labeling Alzheimer’s as type 3 diabetes of the brain.

Key questions prompting debated include:

  • Does insulin resistance provoke Alzheimer’s or do the characteristic protein pathologies accumulate independently?
  • If insulin insensitivity contributes to dementia, what incites this to manifest selectively in the brain versus whole body like usual diabetes?
  • Can addressing cellular starvation from neuronal insulin resistance provide meaningful benefit once substantive neurodegeneration already exits?
  • Do drugs like insulin nasal sprays merely temporarily boost cognitive scores without halting neurodegenerative decline?

Additionally, leading alternative hypotheses argue:

  • The brain shows insulin resistance and glucose hypometabolism as an effect of Alzheimer’s molecularpathology rather than the cause – still unclear.
  • Removing amyloid as the prime target may make metformin and insulin moot by eliminating the root provocateur they react to.
  • Fixing metabolic dysfunction cannot recover destroyed synapses and dying glial support cells needed for cognition regardless of insulin spikes.
  • Controlling cholesterol, exercise and reducing inflammation matters more by improving amyloid clearance and vascular flow than correcting insulin indexes alone.
  • Diabetes and Alzheimer’s prove correlated more from accelerated vascular aging rather than molecular commonalities of cellular starvation, argued some gerontologists.

In effect, the specificity of insulin deficiency independently precipitating neurodegeneration remains disputed by experts espousing amyloid oligomers, prion cascade effects, lipid dysfunction and microbleeds as more direct dementia catalysts.

Nonetheless, the weight of epidemiological data on lifestyle and cardiovascular risks indicates shared pathways exist where insulin deficiency stems from and contributes to escalating neurological dysfunction – supported by PET imaging showing resistant glucose uptake across Alzheimer’s disease stages though still correlative.

This substantiates implementing type 2 diabetes prevention approaches like diet, activity and vascular risk modification in the aim of maintaining cognitive function with aging per many experts.

We’ll analyze specific lifestyle strategies next.

dementia is now known as type 3 diabetes 3

8 Lifestyle Strategies to Reduce Diabetes and Dementia Risk

Until disambiguated by further multicenter trials targeting insulin dysfunction and corroborating pathology in demented brains, the public health sector largely endorsed non-pharmacological prevention techniques for lowering incidence of both type 2 diabetes and Alzheimer’s disease simultaneously given their overlapping epidemiology and clinical features.

These include:

Reducing Processed Carbohydrates

Excess sugar, white flour and processed snacks flood the system provoking chronic blood sugar spikes and inflammation while denying essential nutrients, fiber and fatty acids to nourish 80 billion neurons – accelerating dysfunction.

Increasing Interval Movement

From just 5 minutes of daily stair stepping to 30 minute walks, bursts of cardiorespiratory and resistance activity combat insulin resistance, stimulate microvascular flow and support executive networks in the brain under siege.

Managing Sleep Deficits

Attaining 7-9 hours of recuperative nightly sleep balances hormone cascades that underpin amyloid production and metabolism via the brain’s waste clearance system which relies on sleep.

Stress and Anxiety Reduction

Brain-reactive stress hormones like cortisol directly render insulin receptors insensitive while triggering fight or flight reactions that provoke vascular aging including cerebral bleeds now tied to later dementia.

Prioritizing Produce and Anti-Inflammatory Foods

Abundant colorful fruits, vegetables, legumes, nuts, seeds, fish and healthy fats deliver antioxidants, micronutrients and fiber essential for vascular and metabolic health and optimal neurological function.

Frequent Social Interaction and Novelty

Regular interpersonal exchange builds cognitive resilience by flexing essential social/emotional circuits and promoting new learning repeatedly shown to delay onset of impairment.

Supplementing Key Mitochondrial Nutrients

Several B vitamins, magnesium, acetyl-l-carnitine and alpha lipoic acid help restore neuronal power plants reversing deficits while protecting vascular flow to the hippocampus – outperforming placebo for mild cognitive impairment.

Optimizing Cardiometabolic Biomarkers

Rigorously controlling blood pressure, lipids, insulin, and homocysteine thwarts systemic and neuro inflammation, microbleeds, amyoidogenesis and metabolic waste buildup by improving clearance systems active during deep sleep.

While research continues probing direct causality and molecular timelines, maintaining metabolic, immune and vascular health through lifestyle modulation likely delays disability or death stemming from highly prevalent age-related diabetes and dementia disorders.

Prioritizing behavioral risk reduction strategies offers lasting rewards with few downsides beyond dedication. But medication augmentation may assist those struggling initially with wholesale habit overhauls where small incremental steps fail to budge clinical markers.

Emerging Alzheimer’s Treatments Targeting Insulin & Metabolism

While the field awaits breakthroughs in amyloid, tau protein and neuro-protective domains from over 400 drug trials underway targeting dozens of pathways, progress continues from leveraging diabetes medications that additionally seem to benefit aspects of cognition.

Here is a preview of leading type 2 diabetes and insulin-centric therapies showing promise:

Insulin Nasal Sprays – Following small studies indicating boosting brain insulin availability directly via nasal inhalation temporarily improved memory scoring, current larger trials administer it daily resembling meal timing insulin spikes to determine enduring behavioral or Alzheimer’s biomarker impact.

Intranasal Glucagon-Like Peptide 1 (GLP-1) – Injectable diabetic agents like Byetta already assist glucose control through boosting insulin output while suppressing appetite. Now synthetic GLP-1 nasal sprays aim to bypass the blood brain barrier activating insulin receptors on neurons directly to clear amyloid and correct uptake deficiencies in AD models.

Metformin – This extensively used and generally safe diabetes drug switches metabolism toward more efficient glucose utilization broadly by activating AMP kinase – an effect possibly benefiting cerebral flow and energetics. Ongoing trials are examining metfornin’s effect on cognition in mild to moderate Alzheimer’s patients without diabetes.

Peroxisome Proliferator-Activating Receptors (PPAR) Agonists – While past generation PPAR-gamma and alpha/delta activators failed to clearly slow cognitive loss, newly engineered variants allow 1000x dose escalations in CNS tissues to potently reverse insulin resistance, inflammation, amyloidogenic enzymes and cholesterol transport – holding hope for rivaling expensive antibodies under development to ablate Alzheimer’s pathology directly.

Sodium-Glucose Cotransport 2 (SGLT2) Inhibitors – Alongside GLP-1 class agents, these newer extremely well tolerated diabetes pills leveraging kidneys to flush out blood sugar may potentially reduce systemic and neuro-inflammation driving brain insulin receptor inactivation by eliminating glycemic toxicity and metabolic waste products while enhancing vascular resilience and longevity through pleiotropic impacts – now under international investigation for preserving cognition based on promising epidemiological data.

In summary, an arsenal of therapeutic strategies now take aim at pathways shared by Alzheimer’s with the metabolic syndrome and diabetes in attempt to clear protein toxicities or circumvent accumulating brain insulin resistance – while addressing dementia risk factors like diet, activity, sleep and stress remain foundational.

Now let’s examine specific lifestyle steps individuals can take to lower risk.

10 Immediate Lifestyle Precautions Against Diabetes & Dementia

Until future biological insights parse causation from correlation between disrupted metabolism and escalating cognitive decline, sensible wellness precautions provide lasting rewards whether diabetes or dementia arise.

Here are 10 daily lifestyle precautions against insulin resistant disorders of aging:

Skip Added Sugary Foods and Beverages

Limit concentrated simple carbohydrates provoking inflammation and blood sugar spikes through eliminating candy, desserts, sugary cereals and beverages as habitual parts of your diet.

Choose Good Carbs from Whole Foods

Instead prioritize getting 45-60% of daily calories from fiber-rich complex carbs like non-starchy vegetables, berries, nuts, seeds, beans/legumes and 100% wholegrains which provide steady glucose energy and nutrition.

Prioritize Anti-Inflammatory Fats

Emphasize plant oils like olive and avocado plus oily fish that supply essential fatty acids and polyphenols which improve tissue insulin sensitivity while protecting vascular endothelium – better than animal fats devoid of micronutrients.

Hydrate Amply with Water

Drink sufficient fluids daily from water predominantly while limiting sugary drinks or excessive alcohol known to dehydrate cells, exacerbate inflammation, starve cognition of B vitamins and promote excess calorie intake.

Walk Frequently

Make movement a routine medicine through at least 30 minutes daily of sustained moderate intensity aerobic activity like walking known to slash diabetes and dementia risk powerfully – especially when over 10,000 steps daily.

Incorporate Both Resistance and Cardio Training

For optimal brain and metabolic health, blend in 2 to 3 sessions weekly of strength training along with routines raising heart rates through cycling, swimming, rowing or jogging to build robust circulatory capacity through enhanced vascularization.

Prioritize 7 to 9 Hours Nightly Sleep

Protect cognition and insulin sensitivity by consistently getting at least 7 hours nightly sleep and optimally 9 to allow needed memory consolidation during deep and REM dream states.

Learn and Relax Your Mind Daily

Read, take courses and master new skills routinely to build cognitive reserve while relaxing consciously through yoga, music immersion, nature exposure, meditation or massage to curb cumulative stress effects that accelerate insulin resistance.

Supplement Key Micronutrients

Those over 50 should consider daily supplementation shown to benefit cognition and metabolic factors including vitamin D, marine omega 3s and targeted levels of magnesium, B vitamins like folate, bioflavonoids and vitamin E – best obtained through whole food sources initially.

Embrace Social Connection

Prioritize and enjoy routine socializing, intimate bonding and purposeful endeavors enhancing mood and neural connectivity – pathways repeatedly tied to delayed dementia onset and lower diabetes risks through positive psychological influences.

While no guarantees exist against two of the most challenging epidemics facing aging societies today, embracing research supported lifestyle tweaks pays lifelong dividends supporting vitality across the lifespan.

Now let’s recap key lessons regarding type 3 diabetes links to Alzheimer’s disease.

Conclusion and Summary

  • Substantial epidemiological, pathological and interventional evidence continues substantiating links between systemic metabolic health and later dementia risk – especially type 2 diabetes posing 50-100% greater cognitive threat over time through vascular, structural and neuroinflammatory channels not fully defined.
  • The proposed descriptive terminology of Alzheimer’s as type 3 diabetes tries encapsulating the apparent insulin resistance features selective to memory centers in the brain driving gradually accumulating damage to neuronal health and communication capacity despite most retain stable weight and normal peripheral glycemic control until late stages of neurodegeneration.
  • Yet ambiguity persists whether cerebral insulin deficiency represents an initiating or amplifying feature in Alzheimer’s characteristic pathology and if improving glycemic control can provide more than transient cognitive benefits once extensive amyloid plaques or tau tangles take hold.
  • Nonetheless, committing to known diabetes and heart disease prevention tactics via whole food nutrition, regular movement, stress reduction sleep prioritization pays lifelong dividends for enhancing insulin sensitivity and vascular resilience – brain health being no exception.
  • Emerging drug trials targeting neurometabolic pathways common in both Alzheimer’s and diabetes help CMDT MEDICATIONS (insert cross reference) weiter operationalize potential mechanisms bringing the two together.
  • Yet absent reliable diagnosis or effective intervention for those already exhibiting extensive beta amyloid brain pathology heralding substantive memory loss, stallation of cognitive deterioration remains paramount through modifiable lifestyle andvascular threat reduction for the 1 in 3 lifetime dementia risks ahead.

In summary, likening Alzheimer’s as type 3 diabetes manifesting in nervous system tissues synthesizes the overlapping epidemiological and biological susceptibility pathways degrading cell health in both highly consequential disorders of aging. This framing further spotlights the unrealized power lifestyle and emerging pharmacological factors retain to curtail their shared mortality risks in societies surviving longer yet too often not better.

Until soluble triggers definitively incite or therapeutics reliably arrest the array of protein pathologies and calcium dysregulation obliterating delicate memory circuits, mitigating metabolic, inflammatory and microvascular dysfunction remains paramount against two of the most prevalent and feared syndromes of modern longevity.

Frequently Asked Questions

If I have prediabetes or diabetes does that mean I will definitely get Alzheimer’s dementia too?

While diabetes that is poorly controlled substantially elevates your lifetime Alzheimer’s risk 2 to 5 fold through instigating vascular damage and biochemical stresses taxing the brain, well managed blood sugar and cardiovascular health still proves paramount for circumventing cumulative brain effects. Committing to daily movement, whole food nutrition and involved social engagements offers enduring cognitive resilience too.

Do insulin nasal sprays used for treating Alzheimer’s also help reverse diabetes?

No, deposited intranasally, insulin travels via nerve channels directly accessing brain cells but does not appreciably enter general circulation to assist diabetic control meaningfully like subcutaneous injection. So nasal administration enables bypassing the blood brain barrier to try nourishing dysfunctional memory centers locally. Tablet medications, diet and activity remain necessary to manage most diabetes cases separately.

I read treating Alzheimer’s with metformin could help – but should I ask for this as a 65 year old with normal blood sugar levels?

Emerging but limited and inconsistently replicated research suggests the very commonly used oral diabetes medication metformin might benefit aspects of cognition like processing speed by optimizing insulin signaling, inflammation and energetics. But as risks generally remain low with good kidney function, exploring this off label use possibility with your clinician seems reasonable for noticeably declining focus or memory capacity especially if other lifestyle efforts fail to stabilize progression.

My father has worsening Alzheimer’s disease – would following a very low carbohydrate or ketogenic diet help slow his ongoing memory issues?

Once substantiated pathology propagates causing apparent impairment, radically restricting total carb intake lacks solid clinical evidence for reversing neurodegeneration though offers little risk under supervision. Focus remains on ensuring adequate caloric and micronutrient intake to avoid weight loss while reducing glycemic flux. Support groups and purposeful reminiscence activities often provide more cognitive meaning once extensive loss already mounts.

Does the type 3 diabetes theory definitively prove Alzheimer’s arises from insulin deficiency and metabolic dysfunction alone?

No, the precise origins provoking most common late onset Alzheimer’s pathology still garner debate and may prove multifactoral – with insulin insensitivity acting as an amplifying rather than exclusive culprit through perpetuating inflammation, vascular aging and protein aggregation across already vulnerable neurological networks. Nonetheless, therapeutics targeting intransigent metabolic disorders may offer symptomatic relief.

Final Cognitive Health Strategies

  • Work closely with your medical team to optimize management of cardiometabolic risk factors like portion sizes and blood pressure – what’s good for the heart aids the brain too.
  • If memory concerns arise, obtain structured cognitive testing over time to quantify changes while identifying potential reversible causes of impairment beyond neurodegenerative illness.
  • Explore engaging evidence-based brain wellness programs combining physical activity, cognitive engagement, nutrition and positive social ties – dozens exist locally to globally.
  • Be judicious about allowing news or media outlets to overstate euphoric claims regarding dementia cure breakthroughs typically lacking longer term clinical validation. Tempered optimism serves best.
  • Consider enrolling friends and family in culture change efforts eroding cognitive health stigmas while promoting participation in research efforts hastening therapeutic progress for the billions projected to face Alzheimer’s and dementia in coming generations absent forceful mobilization today.
  • Try focusing less on pathological proteins largely beyond personal control and more daily lifestyle tweaks benefiting whole body and brain health simultaneously – a theme unifying therapeutic quests against diabetes through dementia alike.
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