Is Alzheimer’s Really Type 3 Diabetes? An Evolving Scientific Concept

March 21, 2024

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A silent epidemic of Alzheimer’s disease and related dementias continues ballooning as humanity extends average lifespan further than ever before in history. Today over 50 million people worldwide suffer from dementia induced disability with staggering economic and emotional costs. And over 130 million may develop neurocognitive impairment by 2050 if therapeutic breakthroughs remain elusive against one of medical science’s most enigmatic scourges.

Yet illuminating insights recently emerged recognizing Alzheimer’s extensive overlaps with another global health menace–type 2 diabetes–which likewise counts over half a billion afflicted today linked to modern urbanized lifestyles.

This recognition of pathological and epidemiological similarities between diabetes and dementia has prompted proposals for reclassifying Alzheimer’s as type 3 diabetes: a disease arising from impaired insulin signaling and glucose metabolism but selectively attacking the brain.

But does the evidence truly support labeling Alzheimer’s an isolated diabetic condition destructive to memory centers? Can lessons from diabetes prevention and treatment paradigms unlock future progress halting neurodegeneration?

In this comprehensive guide, learn how experts make the case for Alzheimer’s as a form of type 3 diabetes–along with analyzing skepticism on both sides of an evolving scientific debate full of therapeutic promise. Discover lifestyle tips with demonstrated power to promote cognitive and metabolic health against two of the most pressing disorders of aging.

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Table of Contents

The Creeping Impact of Diabetes and Dementia Worldwide

The 21st century brought with it an explosion of chronic lifestyle mediated diseases–most notably obesity, cardiovascular disease, type 2 diabetes and Alzheimer’s dementia. All stand poised to strain healthcare systems and shorten lifespans if unchecked.

In step with dietary shifts embracing more high calorie yet nutritionally depleted ultra-processed foods across entire nations, both diabetes and Alzheimer’s prevalence swelled simultaneously over recent decades. Today for example:

  • Over 37 million Americans have diabetes–approaching 1 in 10–with equal numbers yet undiagnosed while 96 million battle prediabetes.
  • 11% of US adults over age 65 suffer from Alzheimer’s dementia today skyrocketing to an expected 22% by 2050 absent effective interventions, with financial tolls soaring over $321 billion currently.
  • Globally over 55 million people suffer from dementia presently–a number anticipated to triple in coming decades.
  • Type 2 diabetes results in over 1.5 million deaths annually making it one of humanity’s leading killers.

Yet perhaps most concerning is the consistent clinical relationship repeatedly demonstrated between diabetes and accelerated cognitive decline pointing to fundamentally related underlying drivers.

The Alzheimer’s and Diabetes Connection

Beyond sharing modern lifestyles as disease catalysts, diabetes and Alzheimer’s appear biologically interrelated based on large scale neurocognitive evaluations finding those battling type 2 diabetes substantially prone to dementia progression at disproportionate rates.

For example major studies confirm:

  • 65% of Alzheimer’s patients demonstrate abnormal glycemic regulation or outright diabetes upon testing.
  • Those with diabetes see cognitive faculties deteriorate 2-5 times faster.
  • Vascular dementia risk doubles.
  • Diabetic medications like metformin increasingly tie to lower AD progression after diagnosis in large data analyses.

Autopsies of Alzheimer’s patient brains further demonstrate pathology resembling diabetic complications in critical areas like the memory encoding hippocampus with patterns of:

  • Chronic Brain Inflammation – Both diabetes and Alzheimer’s brains show rampant immune overactivation degrading surrounding tissues.
  • Vascular Dysfunction – Like diabetic kidneys or retinas, the delicate web of cerebral blood vessels nourishing 80 billion neuronal synapses become inflamed, obstructed and leaky early on preceding measurable disability.
  • Neuronal Insulin Resistance – Mirroring cells elsewhere blocking glucose absorption, PET brain imaging confirms impaired glucose metabolism reflecting transport barriers plus deficient insulin signaling within hippocampus and supportive glial cells especially.
  • Mitochondrial Dysfunction – The cellular “power plants” generating ATP chemical energy slow and spark damaging oxidative stress from deficient nutrient availability and inflammatory blocks on glucose breakdown pathways in both diabetes and Alzheimer’s.
  • Cerebral Microbleeds – Gradually accumulating tiny hemorrhages from ailing cerebral blood vessels now appear years before observable cognitive loss–similar to micro-strokes plaguing diabetic organs over time.

This spectrum of evidence interlaces Alzheimer’s pathology with processes simultaneously eroding cells across bodily tissue in those with diabetes, yet concentrating destructive effects in vulnerable memory regions of the brain selectively.

Hence the provocative terminology proposed of Alzheimer’s disease as type 3 diabetes: a disease of systemic metabolic dysfunction sparing the pancreas yet uniquely damaging the master neural networks governing recall capacity plus personality over time through chronic energy imbalance and inflammatory duress exacerbating neuronal loss.

Next let’s analyze the conceptual model behind this terminology in more detail.

The Hypothesis of Alzheimer’s as Type 3 Diabetes

The descriptive framing of most common, non-genetic Alzheimer’s dementia as an isolated endocrine disorder of neuronal insulin signaling–hence type 3 diabetes–first took hold over 15 years ago through compelling academic papers published by research leader Dr. Suzanne de la Monte at Rhode Island Hospital and Brown University.

Her group’s analysis suggests Alzheimer’s excess injury targeting memory centers results from a process that resembles diabetes progression in other delicate tissues–only manifesting through incremental brain glucose and insulin utilization failures selectively crippling cognition rather than the pancreas which continues compensating at the expense of cerebral functions in type 3.

The Underlying Premise Behind the Hypothesis Includes:

  • The brain depends profoundly on insulin signals to uptake blood glucose supplying most all energy needs–yet has far less capacity to synthesize insulin itself compared to the pancreas, relying more on transport from circulation.
  • With aging, rising inflammation coupled to modern dietary and metabolic shifts render transporters along the blood-brain barrier increasingly resistant to shuttling glucose and insulin to needy neurons – initiating gradual uptake dysfunction decades before diagnosable impairment.
  • As cognitive insulin resistance mounts, the hippocampus and supportive glial cells lose efficiency taking up and metabolizing glucose for normal energetic and neurotransmitter balance–eventually starve.
  • Attempts at compensating for accumulating insulin-glucose transport blocks grow inadequate over years, depleting neuronal mitochondria, kindling vicious inflammation and oxidative stress while sparking pathogenic misfolded proteins like amyloid plaques and tau tangles piling up.
  • The unrelenting metabolic crisis prunes synaptic connections provoking personality changes plus memory failures typically emerging subtly then accelerating – clinical hallmarks of recognizes Alzheimer’s dementia.

This hypothesized model proposes insulin deficiency and inflammation drive Alzheimer’s neurodegeneration similarly to damage inflicted on bodily organs in classical diabetes, though constrained to the central nervous system preferentially from lifetime dietary lifestyle factors and genetic risks.

Next let’s break down the stepwise sequence from early risk to diagnosable dementia according to the type 3 model.

alzheimers is diabetes 3 3

Cascading Metabolic Crisis Underlying Alzheimer’s (Type 3 Diabetes)

Just as prediabetes arises when higher yet still sub-clinical blood glucose hints at creeping insulin resistance years before disease thresholds meet diabetes diagnostic criteria, the type 3 model contends neurocognitive insulin resistance subtly emerges up to 20 years ahead of clinically defined Alzheimer’s dementia measurable through emerging biomarkers and subtle cognitive changes.

Here is the hypothesized stepwise sequence:

Stage 1: Cerebral Insulin Resistance Emerges

  • Excess sugar intake strains transport while inflammation renders neuron membranes partially blocking to insulin and glucose transfer from circulation into cells.

Stage 2: Compensatory Hyperinsulinemia

  • Rising systemic insulin output tries overcoming receptor resistance, flooding already glucose flooded cells and circulation provoking vascular injury underlying microbleeds and strokes.

Stage 3: Neuronal Energy Crisis Ignites

  • Despite temporal insulin excess, cells chronically starve from glucose failing cell entry, exhausting mitochondria and sparking oxidative stress plus inflammation from accumulating waste like amyloid beta peptides directly toxic while kindling cytokine storms.

Stage 4: Synaptic Network Breakdown

  • With neuron communication now faltering from energetic deficiencies, misfolded proteins degrade supportive glial cells and synaptic architecture – depression and apathy follow.

Stage 5: Recall Networks Collapse

Vulnerable memory circuits like the hippocampus and frontal executive centers atrophy, devastating cognition as personality simultaneously erodes from accumulated waste, vascular injury and cell loss decades in the making.

If precise drivers prove analogous to pancreatic burnout in classical diabetes, the emphasis on preventing and reversing cerebral insulin resistance early could profoundly impact Alzheimer’s disease course according to experts espousing type 3 hypotheses.

Promisingly, behavioral interventions like nutrition and physical activity that prevent diabetes demonstrate reproducible benefits against cognitive decline in large studies – consistent with shared pathology.

Let’s analyze some of that compelling evidence next.

7 Supporting Lines of Evidence for Alzheimer’s as Type 3 Diabetes

Beyond the apparent pathological evidence in post-mortem evaluations supporting cerebral insulin resistance and metabolic crisis underlying Alzheimer’s neurodegeneration, additional population and clinical clues continue substantiating potential accuracy of the type 3 diabetes model according to proponents like Suzanne de la Monte.

Here is a sample of consistent research threads she and collaborators highlight:

1. Diabetes Treatment Lowers Dementia Progression

  • Metformin and other anti-diabetic medications correlating to better glycemic control significantly associate to lower Alzheimer’s advancement compared to those with diabetes alone in very large retrospective analysis of insurance records encompassing over a quarter million aging adults followed for 6 years on average.

2. Pre-Diabetes Multiplies AD Risk More Than Vascular Dementia

  • Having higher yet not formally diabetic glucose measurements doubles future Alzheimer’s likelihood (but not vascular dementia) in a decade plus long cardiovascular study – implicating early metabolic syndrome especially driving Alzheimer’s pathology selectively.

3. Cerebral Atrophy Maps Diabetes & Alzheimer’s Progression

  • As diabetes control and duration increase, so does the extent of gray matter volume loss in AD prone areas like hippocampus, precuneus and temporal lobes on MRI scans indicative of accelerated neurodegeneration.

4. Diabetes & Alzheimer’s Gene Cluster Risks Overlap

  • DNA screening reveals genomic vulnerability markers for both diabetes and Alzheimer’s concentrating around neuronal insulin activity, brain inflammation and cholesterol processing rather than amyloid or tau variants – consistent with the metabolic disorder model.

5. Human Diabetic Nerve Cells Display Alzheimer’s Pathology

  • Inducing hyperglycemia to mimic diabetes progression in human nerve cells grown in laboratories is sufficient to spark Alzheimer’s type oxidative damage, amyloid oligomer accumulation and deterioration within weeks directly from metabolic duress absent other genetic risks.

6. Correcting Insulin Signaling Reverses Memory Loss Symptoms

  • In animal models of Alzheimer’s pathology, three weeks of insulin sensitizer drug therapy completely reverses memory loss and oligomer deposition to control levels indicating the necessity of insulin signaling maintenance against progressive impairment.

7. Ketogenic Diets Protect Mice From Alzheimer’s Risks

  • While extremely low carbohydrate, high fat ketogenic diets can risk kidney health in humans if not carefully implemented under guidance, rodent modelling finds such regimens suppress brain inflammation and insulin resistance provoking most hallmark Alzheimer’s pathology by stabilizing energetics independent of dietary glucose access.

Such multifaceted results continue substantiating potential for an intransigent metabolic imbalance at the roots of sporadic Alzheimer’s in the context of modern obesogenic diets and lifestyles – with inflammation and cerebral insulin dysfunction proving integral to the stealth destruction of personhood and memory from neuronal energy deficits accumulating over decades.

Yet ambiguity and debate still shroud the type 3 diabetes model for Alzheimer’s looking ahead.

Controversies Around the Type 3 (Alzheimer’s) Diabetes Hypothesis

Despite the epidemiological, genetic, physiological and anecdotal clues supporting Alzheimer’s as a form of isolated brain diabetes – whether accurately labeled type 3 diabetes or not – ample skepticism and uncertainty persists in several corners of the scientific community.

Key questions posed by critics include:

  • Does cerebral insulin resistance actually initiate Alzheimer’s pathology or merely amplify independent neurodegenerative processes like amyloid oligomer toxicity?
  • Can addressing metabolic dysfunction meaningfully slow dementia once extensive tau pathology or neuronal loss manifests?
  • Do intranasal insulin trials only temporarily boost cognition without benefiting disease course?
  • Do genes linked to insulin signaling and cholesterol balance contribute more indirectly than amyloid promoters like APOE4 variants now Questioned by some?
  • Does vascular aging from cardiovascular risks like smoking and inactivity damage cognition more than insulin deficiency alone?
  • Are promising diabetes medications like liraglutide just masking symptoms or stalling microscopic disease advancement?
  • Should ketosis inducing regimens balance potential benefits against kidney health risks?
  • Could amyloid possibly induce insulin resistance or micro bleeds as an earlier primary culprit enhanced by hyperglycemia only later secondarily?

In summary, while the role of cerebral insulin and metabolic deficiency stands increasingly probable as amplifier and correlate to Alzheimer’s disease pathology by diverse experts aligned with type 3 diabetes models, others argue earlier instigators of amyloid tangles or neurovascular injury better explain total disease progression.

Without more advanced imaging illuminating sequential pathology timelines plus clinical trials targeting insulin signaling years before impairment, ambiguity around precise causation remains according to critics.

Nonetheless, most researchers agree lifestyle and emerging pharmacology targeting shared risk pathways between diabetes and dementia deserve prioritization for tangible clinical benefits with minimal side effects given disastrous projections absent therapeutic gains.

Next we’ll break down some of those key strategies showing promise.

7 Daily Lifestyle Precautions Against Diabetes & Dementia

Until therapeutics like insulin nasal sprays or anti-inflammatory diabetes treatments definitively prove capability to reverse extensive Alzheimer’s pathology after diagnosis – which remains unlikely – prevention of metabolic and vascular risk factors through daily lifestyle tweaks offers lasting cognitive and health rewards while advancing science works toward cures.

Here are 7 daily precautions with benefits against diabetes, dementia and beyond:

1. Reduce Processed Carbohydrates

  • Limit concentrated sugars, refined grains and calorie dense processed snacks improving glycemic control while fighting inflammation underlying insulin resistance and micro bleeding.

2. Walk & Strength Train Most Days

  • Movement combats metabolic syndrome and hormone imbalance while improving blood vessel and muscle fitness essential for stable cognition and reducing diabetes likelihood long term.

3. Calibrate Portion Sizes

Achieving moderate caloric balance helps sustain energetic homeostasis and cell repair capacity through nutritious whole food sources rich in brain protective compounds absent most packaged products.

4. Prioritize 7 to 9 Hours Nightly Sleep

  • Restorative sleep enables memory consolidation and cognitive resilience while regulating metabolic hormones plus cleaning toxic byproducts driving cell injury underlying insulin resistance over decades.

5. Engage Socially and Intellectually Daily

  • Sustained interpersonal engagement, curiosity and intellectual challenge buttresses essential neural networks combating isolation and depression that speed metabolic syndrome and neurodegeneration.

6. Manage Life Stresses Skillfully

  • From sufficient sleep and socializing to mindfulness practice and talk therapy, keeping anxiety and depression from runaway metabolic consequences requires active stress modulation life long.

7. Obtain Early Screening If At Risk

  • Those with diabetes, pre-diabetes, heart disease risk factors, family dementia history or even subtle cognitive changes deserve regular neurological evaluations to uncover reversible causes of impairment early plus precisely advise lifestyle steps and emerging treatment options as applicable.

While research continues evolving most effective clinical protocols targeting pathologies like amyloid beta, achieving daily balance across whole body health parameters pays the most reliable dividends long term by supporting optimal aging.

Now let’s examine leading drug candidates showing early promise against Alzheimer’s focusing heavily on metabolic factors.

6 Leading Drug Candidates Targeting Metabolism Against Alzheimer’s

Pharmaceutical developers continue targeting dozens of pathways from amyloid vaccinations to anti-inflammatory monoclonal antibodies seeking to slow or arrest pathology in those displaying early stage impairment.

Yet a subset of promising therapies leverage proteins and pathways integral to glucose regulation, insulin signaling, energetics plus micro bleed prevention – consistent with metabolic syndrome models like type 3 diabetes risking Alzheimer’s.

Here are 5 leading drug candidates taking aim at metabolic or vascular components:

1. Intranasal Insulin

  • Attempting to bypass the blood-brain barrier through direct nose to brain insulin administration aims to stimulate cerebral glucose consumption while clearing amyloid peptides. Results remain preliminary.

2. Injectable GLP-1 Agonists

  • Already assisting diabetes treatment, GLP-1 mimics like Victoza now show measurable benefits against cognitive loss while suppressing appetite helpful for weight reduction – critical given obesity’s role provoking cognitive insulin resistance.

3. Metformin & Other Sensitizers

  • This widely used and well tolerated diabetes drug activates AMP kinase – a key cellular enzyme regulating inflammation, circadian rhythms, protein recycling and vascular flow holding promise for multiprong benefits slowing neurodegeneration.

4. PPAR Agonists

  • While past PPAR candidates failed for Alzheimer’s treatment, newly optimized compounds successfully penetrate the blood barrier at sufficient levels in animal models to suppress neuroinflammation and insulin resistance while reducing both amyloid and tau pathologies consistent with metabolic dysfunction instigating Alzheimer’s progression.

5. Antihypertensive Medications

  • Controlling blood pressure definitively reduces micro bleeds while lowering heart attack and stroke likelihood – essential for supporting delicate brain circulation threatened by diabetes associated risks over decades.

6. Cholesterol Targeting Statins

  • Controversial for Alzheimer’s prevention, the weight of evidence confirms vascular and metabolic benefits from moderating lipids likely outweigh risks as part of multi domain lifestyle therapy – with potential cognition advantages emerging among middle aged users showing stability decades later.

In summary, an integrated approach balancing risk factor optimization through nutrition, physical activity, sleep prioritization plus stress management in combination with moderate pharmaceutical augmentation as needed currently offers the best hedge against cognitive and physical declines until breakthrough treatments arrive.

Now let’s examine helpful perspectives for living with uncertainty through a summary of key insights covered.

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Chasing Causation, Facing Reality

Despite thought provoking metabolic and pathological overlaps between type 2 diabetes and typically late onset Alzheimer’s disease burdening over 100 million aging individuals today, the precise origin of most dementia remains stubbornly elusive – with both lifestyle and genetic contributors conspiring insidiously through still ambiguous timelines.

Like the famed parable of blind men grasping different extremities of an elephant each declaring wholly distinct animals based on their isolated experience, contemporary researchers continue grappling over sized chunks of disease pathology seeking definitive triggers that likely prove multifactoral.

Yet fruitlessly chasing elusive cures decades too late for those already exhibiting extensive irreparable neurological injury risks fostering nihilism or inaction among proactive individuals today.

Instead, the integrative type 3 diabetes model distills common risk knowledge into daily precautions realistically shielding susceptibility:

  • Embracing regular activity, stress relief practices and mixed whole food nutrition sways systemic metabolism against diabetes while optimizing cerebrovascular function essential to lasting cognition.
  • Controlling portion sizes, processed carbs and Achieving ideal weight supports hormonal balance lowering dementia risk over decades.
  • Frequent socializing and intellectual engagement builds cognitive resilience by constantly reinforcing essential neural circuitry integrity over years to delay onset of clinical impairment.
  • Managed heart disease risks like blood pressure and diabetes itself defend delicate cerebral blood vessels against silent bleeding from structural fraying worsened by chronically elevated glucose and insulin toxicity over a lifetime.

In essence, lifestyle therapy targeting modifiable risks common to dementia and diabetes remains paramount at any age absent reliable pharmaceutical options for those already exhibiting extensive memory pathology.

Yet for all, including vulnerable APOE4 risk gene carriers better understanding key disease milestones aids reality based planning over years or decades (refer cross reference).

Now let’s recap core lessons for empowering individuals to optimize health behaviors reducing likelihood of surrendering years of quality life to metabolic or memory disorders.

Conclusion and Summary

  • Substantial evidence continues corroborating extensive pathological and epidemiological overlaps between escalating type 2 diabetes and Alzheimer’s disease prevalence as modern life extending longevity collides with obesogenic dietary patterns.
  • The provocative framing of Alzheimer’s as type 3 diabetes manifesting from systemic insulin resistance selectively damaging the brain attempts unifying disease model commonalities with implications for prevention and therapeutic Insights.
  • While skepticism persists whether cerebral insulin deficiency and metabolic disturbances contribute to or merely amplify independent neurodegenerative disease pathways not fully defined, prioritizing lifestyle precautions and emerging pharmaceuticals targeting shared biomarkers between diabetes and dementia earns clinical support absent reliable cure or prevention options today.
  • Achieving regular mixed interval movement, brain training activity, stress and blood sugar management plus nutrition emphasizing whole foods over refined carbs offers lasting rewards against metabolic syndrome threatening global population health and longevity from the cellular to societal levels worldwide. But progress takes time.

Until molecular breakthroughs unravel biological mysteries of dementia for cures tomorrow, persistently patient, proactive individuals leverage self education and lifestyle logging for diminishing inflammatory risks magnifying disability by the decade ahead.

Frequently Asked Questions

My father has worsening Alzheimer’s but his doctor disputes it relates much to well controlled diabetes he battles too – is she behind on the type 3 research?

Only a subset of experts currently endorse the framing of typical Alzheimer’s as isolated type 3 diabetes given unresolved questions around precise pathology timelines and causal relationships confounded by individual variability. But the weight of population evidence supports managing one’s overall metabolic health optimizing chances against progressive dementia through movement, nutrition and vascular precautions regardless of diabetes or genomes.

I’m newly diabetic but my aunt with Alzheimer’s dementia showed no signs of diabetes – doesn’t that contradict the type 3 model?

The hypothesized model of Alzheimer’s as type 3 diabetes centers around lifelong cerebral insulin resistance and metabolic deficiency stress decaying neuronal integrity over decades subsequently instigating memory network collapse selectively. Since pancreas cells often continue excessive insulin output initially before fatiguing as diabetes advances, blood sugar control can paradoxically persist until later dementia stages, supported by diabetic medications masking systemic evidence longer term.

My 70 year old father battles pre-diabetes and some cognitive issues – will metformin and weight loss supplements halt his Alzheimer’s risk now?

Emerging but limited evidence suggests the very safe diabetes drug metformin might benefit aspects of cognition like processing speed in those at higher risk – either from pre-diabetes, obesity or old age – by optimizing insulin signaling, inflammation and bioenergetics without significant side effects. For mild acquired impairment, structured lifestyle therapy emphasizing whole food nutrition, physical activity and mental engagement tactics often helps although consistency with support systems can prove challenging longer term.

Does research definitely prove Alzheimer’s gets prevented through controlling type 2 diabetes?

No definitive clinical trials yet demonstrate diabetes treatment or modulation reliably prevents eventual Alzheimer’s dementia diagnoses longer term across populations but substantial epidemiological data continues substantiating the substantially lower lifetime dementia risk and later onset among aging diabetics achieving stable glycemic control through medication adherence and lifestyle factors – especially including regular movement, ideal weight targets, smoking cessation and blood pressure management.

My aunt’s advancing Alzheimer’s worries everyone in my family. Should we all go on ketogenic diets or take tons of supplements now even without diabetes currently?

In your situations, focusing first on daily movement spans you enjoy, community engagement, stress resilience tactics and whole food nutrition with plants, antioxidants and anti-inflammatory fats suits best over radical ketosis requiring strict discipline. Priority vitamins like activated B12, blood level verified vitamin D and omega 3 intake offer low risk benefits. Larger lifestyle shifts evolve gradually over years. Early memory screening every 1-2 years can verify changes warranting future nutrition or drug considerations.

Final Cognitive Health Strategies

  • Work closely with your medical team to optimize management of heart disease risks like blood sugars, portion sizes and untreated hypertension – what benefits circulation and metabolism aids the brain.
  • If memory concerns arise, obtain structured cognitive testing over time from specialists to quantify changes while identifying potential reversible causes of impairment beyond neurodegenerative processes.
  • Consider enrolling friends and family in culture change efforts eroding cognitive health stigmas while promoting participation in regular community or virtual social engagements and self education efforts which provide lasting enrichment.
  • Focus on each small step towards daily physical activity, intellectual stimulation, stress mastery tactics and dietary quality driving vascular and metabolic health – our most reliable hedge against swift cognitive demise for now. But retain balanced optimism on the journey ahead.
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