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The Fundamental Role of Autonomic Dysfunction and Lactic Acidosis in Alzheimer’s Disease

by Carlos ETB Monteiro(more info)

listed in alzheimer's and dementia, originally published in issue 265 - September 2020


Carlos ETB Monteiro - Independent Researcher and Scientist President, Infarct Combat Project ( ). Fellow, American Institute of Stress

Paul J. Rosch, MD - Clinical Professor of Medicine and Psychiatry New York Medical College; Chairman, The American Institute of Stress ( ). Obituary Tribute to Dr Paul J Rosch MD MA FACP: June 30, 1927 - February 26, 2020 published in Positive Health PH Online Letters to the Editor Issue 262 May 2020

Amazon The Fundamental Role of Autonomic Dysfuntion and Lactic Acidosis

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Acknowledgement Citation

This article by Carlos ETB Monteiro and Paul J. Rosch MD has been published in Autonomic Dysfunction and Lacid Acidosis = Multiple Diseases by Carlos Monteiro. Available on and 


“…. Acidosis may stimulate an extracellular deposition of amyloid and contribute
to the pathogenesis of Alzheimer disease”, Gregory J. Brewer, 1997 [1]



This article discusses recent findings that amyloid-beta peptide is a consequence of acidosis, rather than the initial cause of Alzheimer’s Disease (AD). It postulates that autonomic dysfunction is a precursor of AD because it increases plasma lactate concentrations. This is consistent with the acidity theory of atherosclerosis proposed in 2006, which supports the vascular hypothesis as well as the role of brain lactate production in the progression of AD. Other influences such as digoxin, ketogenic or high fat - low carb diets, choline intake and supplements like Vitamin C, Vitamin D, Vitamin E, Quecertin and Omega-3 are also important, since they may prevent or improve cognitive deficits in AD.  The article also present studies showing that some drugs like beta-blockers and statins as much as diseases like diabetes and coronary artery calcification, may induce cognitive decline.


A study published in 2019 on AD drug development[2] reviewed the website to evaluate all pharmacological agents currently being developed for the treatment of AD. It concluded that:

“The lack of success in AD drug development has given rise to nihilism with regard to the ability of the field to develop agents that meaningfully modify the progression of AD. Suggestions to abandon the amyloid hypothesis, focus exclusively to combination therapies, place more emphasis on lifestyle interventions to prevent AD or reassess our assumptions and build new models to drive drug development are all voiced, and each of these perspectives have merit.”

Other recent studies have also discussed the failure of drugs to treat AD. [3,4,5,6] With respect to the effect of acidosis on amyloid-beta, a recent study[7] noted:

The accumulation of toxic Aβ and p-tau may not be the initial cause of neural degeneration and may instead be consequences of other causative factors. . . .Neurons don’t ordinarily make adaptive and compensatory shifts to glycolysis, including under stress conditions. Instead, they have a high demand for other oxidative substrates and, in particular, lactate, which is largely provided by proliferating astrocytes through their high glycolytic capacity.

Lactate Levels In AD

a)     A 2014 study showed that patients with early AD have higher glucose concentration in an area susceptible to AD pathology compared to controls. In addition, lactate concentration is higher, suggesting greater regional metabolic reliance on glycolysis. These results motivated a longitudinal study of MRS glucose and lactate as novel AD biomarkers [8]

b)     A 2015 study suggests a dynamic relationship between neuronal energy metabolism, tau proteins and cognitive decline in AD and proposes the clinical potential of assessing CSF lactate levels in patients with AD to better define damage to neuronal brain communication. [9]

c)     A 2016 study suggests that during progression of AD, aerobic glycolysis and lactate production may in fact be detrimental and contribute to cognitive decline.[10]

The Vascular Hypothesis Of Alzheimer’s Disease

Evidence from pathological, clinical and epidemiological studies indicates an association between AD and atherosclerotic disease due to a progressive reduction of blood flow to the brain. [11]

Other studies have shown that a severe increase in carotid intimal medial thickness may be considered as a marker for progression of the cognitive decline in AD, and that interventions to reduce atherosclerosis may help to prevent the onset of vascular dementia and AD [12, 13,14]

Jack C. de la Torre, one of the authors of the vascular hypothesis as a cause of Alzheimer’s Disease that was developed in 1993 [15], recently noted:[16]:

“There is growing evidence that chronic brain hypoperfusion plays a central role in the development of Alzheimer's disease long before dyscognitive symptoms or amyloid-β accumulation in the brain appear.”

de la Torre, has also implicated many other cardiovascular risk factors in the development of cognitive impairment preceding AD, including atrial fibrillation, thrombotic events, hypertension, hypotension, heart failure, low cardiac index and valvular pathology.[17] Additional risk factors for AD such as: aging, family history, gender, lifestyle, diabetes mellitus, stroke and genetic influences have also been mentioned in other studies.

What sparked our interest regarding Alzheimer’s disease and its possible association with atherosclerosis was a Medscape report [18] of a study showing that beta-blockers used to treat hypertension resulted in fewer Alzheimer’s type brain lesions than other antihypertensive drugs. The study, which was published in September 2013 [19], involved 774 elderly male Japanese Americans who participated in the Honolulu-Asia Aging Study [20]. Of these, 610 had high blood pressure or were being treated with medication for hypertension. Among those who had been treated (about 350 patients), 15 percent received only a beta blocker, 18 percent received a beta blocker plus one or more other medications, and the rest of the participants received other antihypertensive drugs. It found that all types of treatment to lower elevated blood pressure were clearly better than no treatment. Autopsies were performed on all participants, and men who had received beta blockers as their only blood pressure medication had fewer abnormalities in their brains compared to those who had not been treated for their hypertension, or who had received other blood pressure medications. The brains of participants who had received beta blockers plus other medications showed an intermediate reduction in numbers of brain abnormalities.

These included two distinct types of brain lesion: those indicating Alzheimer’s disease, and lesions called microinfarcts, usually attributed to tiny, multiple, unrecognized strokes. Study participants who had taken beta blockers alone or in combination with another blood pressure medication also had significantly less brain pathology. The association between beta blocker use and cognitive impairment was stronger among men with diabetes aged >75 years and those with a pulse pressure ≥70 mm Hg. [19]

Dr Lon R White, one of the authors of the study, speculated on the mechanisms of action in a Medscape interview [18] in which he noted that beta blockers reduce pulse rate, which might have an effect on small-vessel microinfarcts in the brain, as follows:

“Lifelong exposure of the pulse pressure in the brain might cause some damage," he said. "While we thought beta-blockers may reduce brain microinfarcts, which they did, we actually saw a larger reduction in the Alzheimer's-type lesions, which we had not expected. This is somewhat of a mystery at present and may be a chance finding. But if it is a real effect, I would think it was something to do with autonomic function." White suggested that a reasonable next step could be to test this hypothesis in mice genetically engineered to produce these Alzheimer's lesions. "If we treat these mice with beta-blockers and they develop fewer lesions, then we will know that it is an effect of the drugs.”

The Acidity Theory of Atherosclerosis And The Vascular Hypothesis Of AD

We see some concordance between White’s interpretations and the concept that the autonomic nervous system dysfunction, with sympathetic dominance representing the primary factor in the cascade of events leading to atherosclerosis. The acidity theory of atherosclerosis developed in 2006[21] pointed out that beta blockers, through their sympatholytic effects, have been shown to reduce the progression of atherosclerotic plaques in many studies. It emphasizes that cardiac glycosides like digoxin can also reduce progression of atherosclerosis, [22] which suggests that sympatholytic drugs might also offer some benefits to patients with AD or cognitive deficits.

Do Beta Blockers Cause Cognitive Decline?

Despite studies supporting the beneficial results of beta blockers in AD and dementia, other research suggests these drugs may cause a decline in cognition. For example, a 2007 study investigated the influence of β-blockers on delayed memory function in cognitively impaired patients. The authors concluded that there was a trend for worsened or delayed memory retrieval in patients who were on CNS-active β-blockers. They believe this supports the notion that common medications used in cognitively impaired elderly patients can worsen cognition, and that careful selection of medications may help to prevent this and improve retrieval of newly formed memories.[23]

A  2012 letter commenting on this in J Neuropsychiatry in 2012 [24] concluded:

“There is insufficient evidence for this assertion currently, but further studies should investigate the effects of beta-blockers in patients with cognitive impairment or dementia.”

More recently, a 2016 JAMA study showed that the use of beta-blockers resulted in worsened functional outcomes among nursing home residents with substantial cognitive or functional deficits. The initial cohort of 15,720 patients (11,140 women [70.9%] and 4,580 men [29.1%]; mean age, 83 years) included 8,953 new beta-blocker users and 6,767 nonusers. The propensity-matched cohort included 5,496 new users of beta-blockers and an equal number of nonusers for a total cohort of 10,992 participants. The authors concluded that the use of beta-blockers after acute myocardial infarction is associated with functional decline in older nursing home residents with substantial cognitive or functional impairment, but not in those with relatively preserved mental and functional abilities.[25]

Is Beta-blocker Therapy For Hypertension Dangerous?

1)     A 2005 Lancet paper concluded [26]:

In comparison with other antihypertensive drugs, the effect of beta blockers is less than optimum, with a raised risk of stroke. Hence, we believe that beta blockers should not remain first choice in the treatment of primary hypertension and should not be used as reference drugs in future randomized controlled trials of hypertension.

2)     A 2008 study also found that beta--blocker associated reduction in heart rate increased the risk of cardiovascular events and deaths of hypertensive patients in a meta-analysis of more than 60,000 patients in 9 large beta blocker trials [27]. In subsequent correspondence, the authors suggested that drug-induced bradycardia is less beneficial than spontaneously occurring bradycardia. and may be related to the “dyssynchrony of the reflected pulse wave and the outgoing pressure wave.” [28].

3)     A 2017 Cochrane Database paper concluded that [29]:

Most outcome RCTs on beta-blockers as initial therapy for hypertension have high risk of bias. Atenolol was the beta-blocker most used. Current evidence suggests that initiating treatment of hypertension with beta-blockers leads to modest cardiovascular disease reductions and little or no effects on mortality.

Coronary Artery Calcification and Cognitive Decline

1)     Studies from 2013 and 2014 have reported the reduced pineal volume and have found calcification in AD. [30, 31]

2)     A study from 2015 found that larger calcification volume in all vessels, except in the coronaries, was associated with a higher risk of dementia. Additional analyses for Alzheimer's disease showed similar results. These larger calcification volumes were also associated with cognitive decline. [32]

3)     A study published in 2017 confirmed that higher baseline coronary artery calcification was significantly associated with increased risk of dementia. [33]  

4)     A study published in 2019 has observed reduced pineal gland volume and pineal calcification, accompanied by cognitive decline and sleep disturbances in AD patients. [34]

5)     A recent study postulated that increased lactate production is the responsible for coronary artery calcification. [35]

Diabetes and Cognitive Decline

1)     Data from a large veteran’s registry in the USA from 2011  has shown that, among people with diabetes, the prevalence of dementia and cognitive impairment combined was 13.1% for those aged 65–74 years and 24.2% for those aged 75 years and older. [36]

2)     A study from 2018 provided evidence to support the association of diabetes with subsequent cognitive decline. Their findings show a linear correlation between circulating HbA1c levels and cognitive decline, regardless of diabetic status. The study comprised 5189 participants and the mean follow-up duration was 8.1 ± 2.8 years and the mean number of cognitive assessments was 4.9 ± 1.5. According the authors their findings suggest that interventions that delay diabetes onset as well as management strategies for glucose control, might help to alleviate the progression of subsequent cognitive decline over the long term. [37]

3)     Autonomic dysfunction and raised lactate production are common in Diabetes. [38-40]

Statins and Cognitive Decline

A paper from 2019 analyzed relevant studies of the relationship between cognitive performance and statin and usage. It included articles published between 2018 and 1992. It was identified three randomized trials, one observational study and 66 case reports that provided credible evidence of statin induced cognitive impairment. It also identified seven randomized trials and two observational studies reporting no significant evidence of statin-induced cognitive impairment. This study found methodological differences that may have contributed to the divergence of these results. Evaluation of all these studies indicated that statin-associated cognitive decline is a real entity. Likely mechanisms to explain the adverse effects include 1. Reduction of synthesis of coenzyme Q10 with consequent increasing oxidative stress and reduction of cerebral energy production; 2. Depletion of central nervous system myelin by inhibition of cholesterol synthesis. The authors concluded that statin-induced cognitive decline does exist, needs to be better recognized and requires more studies of prevention and treatment.” [41]

Note: Statin therapy may induce acidosis. [42,43]

Vitamin D Improvement Of Cognitive Function

The neuroprotective effect of vitamin D is likely an important contributor to memory development and preservation of normal cognitive function. [44] Moreover, compared with healthy people of the same age, the plasma 25-D level of AD patients seems to be markedly lower. This suggests that vitamin D may have potential benefits on cognitive function. [45] A recent 2019 study found that oral vitamin D supplementation (800 IU/day) for 12 months may improve cognitive function and decrease amyloid beta-related biomarkers in elderly patients with AD. [46]

Omega-3 Improvement Of Cognitive Function

A 2017 study found that quantitative omega-3 EPA+DHA erythrocyte concentrations are independently correlated with brain perfusion on SPECT imaging and neurocognitive tests. These results have implications for the role of omega-3 fatty acids toward contributing to cognitive reserve. [47]

The effects of omega-3 fatty acids supplementation in mild AD corroborate epidemiological observational studies showing that omega-3 fatty acids may be beneficial in disease onset, when there is slight impairment of brain function.

This systematic review published in 2017 says that although some studies have shown changes in scales of cognitive function in more severe cases, more studies are necessary to confirm the benefit of omega-3 fatty acid supplementation in the treatment of AD. [48]

Improvement Of Cognitive Function With Digoxin

In a NEURO2019 presentation, the authors discussed their observation that digoxin significantly prevented the ICV-STZ (intracerebroventricular-streptozotocin) induced memory deficit by attenuating hippocampal neuronal loss, neuroinflammation and cholinergic deficit in rats. These findings suggest that digoxin might be beneficial for treating AD. [49] A study from 2009 has shown that treatment with digoxin may selectively improve cognitive function in older patients with heart failure. [50]

Increased Choline And Egg Intake Improve Cognitive Function

A recent study found that higher phosphatidylcholine intake was associated with lower risk of incident dementia and better cognitive performance in men in eastern Finland [51]. According to the authors, choline is an essential nutrient that is needed as a precursor for the neurotransmitter acetylcholine, and for phosphatidylcholine, a membrane constituent. They also suggested that choline has a role in the prevention of cognitive decline and Alzheimer disease. In addition, it is an ingredient in a multi-nutrient medical food developed for treating mild AD. These authors previously reported that higher egg intake was associated with better performance in certain cognitive tests and tended to lower risk of dementia [52]. Other studies have also observed a beneficial association between egg intake and cognitive performance. In addition to meat and other animal products, egg yolk is a major dietary source of choline and especially phosphatidylcholine. Consumers of eggs had almost double the usual intake of choline as compared to non-consumers [53].

Another animal study, also published in 2019, demonstrated that lifelong choline supplementation produces profound benefits, suggesting that simply modifying diet throughout life may reduce AD pathology. [54] Acetylcholine is the chief neurotransmitter of the parasympathetic nervous system an important component of the autonomic nervous system.

Quecertin Improvement of Cognitive Function

Several studies have reported on the neuroprotective effects of the flavonoid quercetin, both in vitro and in vivo models of neurodegenerative disorders, such as cognitive impairment. [55]

Some recent studies:

1)     A study from 2015 [56] evaluated the neuroprotective effect of quercetin (25 mg/kg) administration via Intraperitoneal injection every 48 hours for 3 months on aged (21–24 months old) triple transgenic AD model (3xTg-AD) mice. Its data has shown that quercetin decreases extracellular β-amyloidosis, tauopathy, astrogliosis and microgliosis in the hippocampus and the amygdala suggesting it reverses histological hallmarks of AD and protects cognitive and emotional function.

2)     In a study published in 2019 [57], the same group of researchers [56] suggested that preventive and chronic administration of quecertin might help to delay the development of histopathological hallmarks and cognitive function deficits in AD.

Vitamin E and C Improvement of Cognitive Function

A study from 1998 [58] examined the relation between use of vitamin E and vitamin C and incident Alzheimer disease in a prospective study of 633 persons 65 years and older. After an average follow-up period of 4.3 years, 91 of the sample participants with vitamin information met accepted criteria for the clinical diagnosis of Alzheimer disease. None of the 27 vitamin E supplement users had Alzheimer disease compared with 3.9 predicted based on the crude observed incidence among nonusers (p = 0.04) and 2.5 predicted based on age, sex, years of education, and length of follow-up interval (p = 0.23). None of the 23 vitamin C supplement users had Alzheimer disease compared with 3.3 predicted based on the crude observed incidence among nonusers (p = 0.10) and 3.2 predicted adjusted for age, sex, education, and follow-up interval (p = 0.04). There was no relation between Alzheimer disease and use of multivitamins. These data suggest that use of the higher-dose vitamin E and vitamin C supplements may lower the risk of Alzheimer disease.

A study from 2004 [59] found that using both prevalence and incidence data from the large, population-based Cache County study suggest that antioxidant vitamins, specifically the combination of vitamin E and C supplements, may prevent AD. As is widely appreciated, formal proof of such an effect can come only from randomized prevention trials. If proven efficacious in such trials, antioxidant vitamins (believed to offer other health benefits) would offer an attractive prevention strategy for AD. Formal demonstration of their efficacy would therefore have significant public health implications, and we suggest that prevention trials are warranted.

A study from 2017 [60] says: “Ascorbic acid can be considered vital for neuronal repair and offers new molecular mechanisms to understand the true neuroprotective role of AA in brain aging and neurodegeneration”

A study from 2019 [61] found there was a significant association between vitamin-C plasma concentrations and performance on tasks involving attention, focus, working memory, decision speed, delayed and total recall, and recognition. Plasma vitamin C concentrations obtained through vitamin C supplementation did not affect cognitive performance differently to adequate concentrations obtained through dietary intake.

A study published in 2014 told that the relative safety of vitamin E combined with the low cost and the absence of valid alternative treatments for AD, suggest vitamin E as a nutritional compound to promote healthy brain ageing and to delay AD-related functional decline. [62] On the other hand a recent study says vitamin E clinical safety remains controversial and warrants further investigation [63].

Autonomic Dysfunction As A Precursor Of AD

Our present postulate supports both the vascular hypothesis as well brain lactate production in the development of AD. There are numerous studies linking autonomic dysfunction to AD that suggest increased sympathetic and/or decreased parasympathetic activity in AD patients [64-73]. A 2010 study proposed that elevated endogenous brain norepinephrine might be an etiological factor in some patients, and could also accelerate progression of the disease. [74]. Another study found that baroreflex function, which influences sympathetic and parasympathetic activity, is reduced in Alzheimer’s disease.[75]

Risk Factors For Atherosclerosis Consistent With The Acidity Theory

In parallel, it is important to notice the lengthy list of risk factors for atherosclerosis that have dysregulation of the autonomic nervous system as a common denominator. These risk factors were cited in a 2015 paper on the acidity theory of atherosclerosis that included psychosocial factors, diabetes, smoking, air pollution, noise, high carbohydrate diets, vitamin D deficiency, radiation, etc. [22]

With respect to high carbohydrate diets, the article states:

“It is well established that the sympathetic nervous system activity is also influenced by food ingestion, and that diet composition plays an important role. High carbohydrate diets, particularly in the form of high-glycemic carbohydrate, can directly induce endothelial dysfunction, vascular inflammation and subsequent development of atherosclerosis. A study from 2009 advocates that the widespread use of starchy food and sugars has brought a new metabolic problem: a chronically increased sympathetic nervous system activity, where the high glycemic index nutrition has been suggested to play a key role in the pathogenesis of hypertension and atherosclerosis. On the other hand, protein or fat ingestion have no significant sympatho-excitatory effect.”

Trans fatty acid (TFA) – An additional risk factor for AD?

TFA consumption is associated with increased risk of cardiovascular disease as well as a decrease in heart rate variability that reflects autonomic dysfunction [76].  A recent study found that higher serum elaidic acid (an objective biomarker for industrial trans fatty acids) is a possible risk factor for the development of all-cause dementia and AD in later life [77].

High Carbohydrate Versus High-Fat And ketogenic Diets In AD

The literature linking high-fat/low-carbohydrate diet, metabolic ketosis, and cognitive function in the elderly is increasing at a rapid rate. A 2012 paper studied the effects of a high carbohydrate or a very low carbohydrate diet on cognition and mood in mild cognitive impairment (MCI) patients. Only those in the low-carbohydrate group had improved scores on a memory test after 6 weeks; this effect correlated significantly with ketone levels. [78] A 2016 paper reported the effects of diet on risk for dementia in nearly 1,000 older Americans. Senior citizens who normally consumed a high carbohydrate diet had an elevated risk of MCI and dementia, whereas controls with high fat and protein diets had reduced risks [79]

A small 2017 study enrolled 15 AD patients in a non-controlled trial of a ketogenic diet plus a medium-chain-triglyceride fat supplement. Among the 10 who completed the 3-month trial, there was a modest improvement in the Alzheimer’s Assessment Scale-Cognitive subscale. [80] Another study the following year suggested that the protective effect induced by a high fat diet on AD‐like mice, resulted from mechanisms that involve better blood-brain barrier properties and brain morphology (normal ventricle volume, consistent with less brain atrophy) [81]. A more recent paper reported that 14 elderly individuals with mild cognitive impairment consistent with early Alzheimer’s disease, had improved memory and brain function on a high-fat, low-carbohydrate diet.[82]

How Autonomic Dysfunction Leads To Lactic Acidosis

The chronic elevated release of catecholamine release triggered by the sympathetic nervous system can accelerate myocardial glycolysis, which results in a significant increase in lactate production.

The first to observe the influence of adrenaline on lactic acid production were the Coris in the early 1920s. [83]  A 1982 article by Schade provided further support for the direct participation of catecholamines in the development and/or maintenance of lactic acidosis as follows:[84]  

1. The common association of stress and lactic acidosis;

2. The rise in plasma lactate concentration during adrenaline infusion;

3. The precipitation of lactic acidosis by adrenaline intoxication and pheochromocytoma;

4. The vasoconstrictor effects of catecholamines leading to tissue anoxia and lactic acid production.

Risk Factors For Atherosclerosis With Increased Concentration Of Lactate In Plasma That Support The Acidity Theory Of Atherosclerosis.

Elevated blood lactate is associated with increased carotid atherosclerosis.[85] A 1961 study found that that reduction of blood pH increases blood flow. [86] Lowered pH increases perfusion pressure [87,88]. pH changes also have profound effects on the contractility of coronary arteries, [88,89] that may be due to sodium/potassium pump and potassium induced relaxation activities. [90] Lactate, lowered pH and lactic acid induce endocardial damage [91]

The association of increased lipid levels with abnormal lactate metabolism may provide a useful screening test for the detection of coronary artery disease. Plasma lipid abnormalities and myocardial lactate production are significantly associated with subsequent progression of atherosclerosis on arteriography. In addition, the amount of lactate released by the myocardium has been shown to be related to the severity of coronary artery disease. [92-94]

Drugs And Supplements That Inhibit Sympathetic Or Enhance Parasympathetic Effects

Digoxin: [95]
Omega 3: [96]
Vitamin C: [97-99]
Vitamin E [100,101]
Vitamin D: [102]






Diet, Drugs And Supplements That Reduce Lactate/Lactic Acid Production

Digoxin: [105,106]
Ketogenic diet [107]
Omega 3: [108]
Quecertin: [109,110]






Recent Press Release by Blue Cross Blue Shield Association [111] about what we can expect on Dementia and Alzheimer’s disease in the future

It presented the following findings [112]

“The number of commercially insured Americans age 30 to 64 diagnosed with early-onset dementia or Alzheimer’s disease increased by 200% from 2013 to 2017. The average age of a person living with either form of dementia is 49.

These conditions are more common in women, who make up 58% of those diagnosed. Additional findings from the study include:”

  • The number diagnosed with these conditions increased 373% among 30- to 44-year-olds, 311% among 45- to 54-year-olds and 143% among 55- to 64-year-olds from 2013 to 2017.
  • Rates of diagnosis were higher in the East, the South, and parts of the Midwest, while western states showed lower rates of diagnosis.

“The increase in early-onset dementia and Alzheimer’s diagnoses among a generation who typically wouldn’t expect to encounter these conditions for several decades is concerning, especially since there is no cure for Alzheimer’s disease,” said Dr. Vincent Nelson, vice president of medical affairs for BCBSA. “Further education and research is needed to learn more about early-onset dementia and Alzheimer’s, how to treat these conditions and what can be done to better prevent diagnoses.”


We hope, through our postulation and data contained in the present article, to contribute positively in order to avoid that the terrible expectations expressed above by the Blue Cross Blue Shield Association does not turn in reality.


The present article shows a large number of evidences giving support to our postulation about the autonomic dysfunction as the precursor of the process leading to lactic acidosis, the ultimate causal factor for the development of Alzheimer’s disease. Adequate to this new hypothesis are provided solutions for the prevention and possible recovery for the patients affected by this neurodegenerative disease, through specific drugs, diets, vitamins and other supplements which were discussed in this article.


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Acknowledgement Citation

This article by Carlos ETB Monteiro and Paul J. Rosch MD deceased has been published in Autonomic Dysfunction and Lacid Acidosis = Multiple Diseases by Carlos Monteiro. Available on and


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About Carlos ETB Monteiro

Carlos ETB Monteiro is an independent researcher and scientist from Brazil with 43 years’ experience in dealing with medical matters. In 1972 he became a follower in the scientific plan from Dr Quintiliano H de Mesquita, originator of the myogenic theory of myocardial infarction and other pioneer medical contributions (QHM Memorial). In 1999 he participated in the foundation of Infarct Combat Project and elected president by the board of directors. Carlos Monteiro is still supporting Dr Mesquita’s medical and scientific ideas, through Infarct Combat Project. Recently he has developed a new hypothesis to explain atherosclerosis that was named acidity theory of atherosclerosis. The blog new evidences about his Acidity Theory you can find here.

He is a non-official member of "The International Network of Cholesterol Skeptics (THINCS - and Fellow of the American Institute of Stress ( and is also a  member of the honorary board of Weston A Price Foundation ( His recent book Acidity Theory of Atherosclerosis - New Evidences, 2012 is available for Kindle readers and in paperback at  also in paperback. Carlos Monteiro is one of the signatories of a letter to The Academy Obesity Steering Group entitled “Obesity is an Iatrogenic Disease”. He recently presented two lectures in  the Fourth International Conference of Advanced Cardiac Sciences - The King of Organs Conference, 2012, Saudi Arabia: the first about the Myogenic Theory of Myocardial Infarction (Powerpoint presentation and video),  the second about the Acidity Theory of Atherosclerosis (Powerpoint presentation and video). Carlos Monteiro may be contacted via


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