Every year, more and more people lose their minds to Alzheimer’s. A condition not caused by faulty genetics but by environmental factors, leading many to ask, does fluoride lead to Alzheimer’s?
It’s hard to believe, what’s in our water could be damaging our brains…
But the truth about fluoride is that it’s the perfect substance to do so.
What is Alzheimer’s Disease?
Alzheimer’s disease is a progressive, irreversible neurodegenerative disease that is characterized by loss of memory function and other neurobehavioral manifestations.1,2
However, that was an extremely polite description…
The truth is, you slowly lose your grasp on reality.
It’s the disease where in its later and eventual stages, you forget who you are, what you’ve done, and see your children and beloved wife or husband as complete strangers.
It’s not a part of normal aging.
Nonetheless, there are currently more than 47 million Alzheimer’s patients globally, with the number projected to triple to nearly 150 million by 2050.3
What Causes Alzheimer’s?
Currently, only a small percentage of Alzheimer’s cases result solely from genetic mutations.
With most incidents a result of environmental factors, or better put, due to the interaction of environmental factors with pre-existent genetic determinants.4
In other words, whether or not you get Alzheimer’s is in your control.
Here are some of the established risk factors of Alzheimer’s.
It’s through the constant exposure to these risk factors that someone is propelled to Alzheimer’s.
Once enough nights of poor sleep, cups of water with pesticides and toxic ions are consumed, and days the pineal gland does not perform it’s vital functions for your body, is when the early stages of Alzheimer’s emerge.
All of which can be observed through unique characteristics in Alzheimer’s patients.
In general, all the risks and characteristics of Alzheimer’s point to a general theme.
Too much damage to the brain and too little recovery.
Fluoride’s Effect On The Brain?
Unlike many foreign substances, fluoride can cross the blood-brain barrier – giving it freedom to accumulate in the brain and cause widespread damage.5,6,7
Through fluoride’s extremely reactive and toxic nature it carries a well-established prooxidant effect in cells.8 This is the main mechanism that fluoride deploys to cause damage to the central nervous system.
However, fluorides effect on the brain does not stop there.
These are just observations of the effects that took place in the brain of subjects exposed to fluoride.
There are many ways these effects can contribute or cause Alzheimer’s but it’s hard to ignore the effect of “damage to the hippocampus”.
The hippocampus is well known for its role in learning and memory, a key feature Alzheimer’s patients lack.9
But let’s find out what is fluoride and specifically it’s link to Alzheimer’s.
Does Fluoride Lead To Alzheimer’s? (6 Links)
1. Damaged Pineal Gland
There’s no better place to start than fluoride’s effect on the pineal gland.
The pineal gland holds huge responsibility in the body but unfortunately through 3 unique characteristics, it’s quite vulnerable to exposure to fluoride.
Leading to the calcification of the pineal gland.
Once the pineal gland is calcified it becomes in/underactive.
Leaving it unable to perform its role as the body’s primary endocrine organ and main function to synthesize and secrete the hormone melatonin.10
A vital hormone that has been reported to hold multiple roles in the central nervous system, such as improving neurogenesis and synaptic plasticity, suppressing neuroinflammation, enhancing memory function, and protecting against oxidative stress.
This is key to our discussion, as studies have reported reduced pineal volume and calcification in Alzheimer’s patients.11,12
Making a damaged pineal gland the first domino to fall.
2. Decreased Melatonin Production
As fluoride calcifies the pineal gland, the pineal gland begins to produce less melatonin, a factor that is directly associated with the development of neurodegenerative diseases like Alzheimer’s.13,14,15
This is due to melatonin’s vital function in the body.
Melatonin’s main role is to aid in brain health, specifically in the form of:16,17
- antioxidant defense
- immune response
- neuroprotective effects
- anti-amyloid effect, and
- anti-apoptotic activity
Most importantly, melatonin’s role as a free radical scavenger in destructive oxidant activities is most important.18 It’s without this important process that the brain of an individual is left with no ammunition to fight the natural and unnatural events occurring in one’s brain.
Specifically, lack of melatonin deprives the resources needed in hippocampal neurogenesis and hypothalamic neurogenesis.19
With that being said, it’s no wonder Alzheimer patients have lower levels of melatonin compared to normal subjects,20 which effects don’t stop there but spread to the quality of one’s sleep.
3. Sleep Disturbances
Of all of melatonin’s functions, it’s role in directly controlling circadian rhythm (the thing that helps you sleep) is most well known.21
Since those with Alzheimer’s have lowered melatonin levels it should be no surprise that this often leads to sleep disturbances. In fact, sleep disorders occur in up to 66% of Alzheimer’s patients.22
Missing out on sleep, in turn robs the body of sleep’s beneficial aspects. Such as tissue repair, improvement of memory consolidation, neurogenesis, and the release of diverse hormones.
Without sleep, researchers have demonstrated the increase of inflammation could boost the risk of neurodegenerative disease onset.23,24 This is one of many reasons why the development of Alzheimer’s is accompanied by changes in lifestyle factors, like sleep disturbance.3
This robs the body, particularly the brain of the opportunity to recharge and recover.
4. Fluoride Increases Oxidative Stress
Oxidative stress is the imbalance between free radical formation and their removal by antioxidants. When you have more oxidative stress that the brain can handle, it leads to damage to the brain – a process that plays a key role in Alzheimer’s.25
Oxidative stress damages all classes of organic molecules in the cells, causing excessive lipid peroxidation and protein oxidation.26,27
It’s as simple as if your brain were able to keep up with the damage, you’d never get Alzheimer’s.
5. Reduced Antioxidant Enzymes
In recent years, it has been recognized that higher levels of fluoride exposure result in neuronal dysfunction by increasing free radicals (oxidative stress) while also reducing the activity of antioxidants enzymes (the things that fight oxidation).28,29
Fluoride not only gives ammunition to the bad guys but takes ammunition from the good guys.
How To Protect The Brain From Fluoride and Alzheimer’s?
Exposure to fluoride sets-up the perfect environment for Alzheimer’s.
Fluoride crystallizes the pineal gland, turning it in/underactive.
This is followed with a decrease in melatonin production, robbing the body of what it would use in the defense of the development of Alzheimer’s. With the lack of melatonin, a person’s sleep is disrupted, robbing them of valuable time to recover their brain.
Aside from the pineal gland’s destruction by fluoride, fluoride directly damages the brain.
It increases oxidative stress and reduces antioxidant enzymes.
This essentially fuels the bad guys with machine guns and gives the good guys rocks.
Fluoride exposure leaves a person’s brain without the resources to fight off brain damage, strips the brain of time to recover, increases destructive activity and decreases protective activities of the brain.
It would be harder to imagine a better environment for the onset of brain diseases.
Now, what’s the solution?
Well, you have to change the environment…
Fluoride Detox To Avoid Alzheimer’s?
In this sense, an ounce of prevention is worth a pound of cure.
Especially since Alzheimer’s is progressive and irreversible…
The only goal here is to avoid it.
The way you can do this is through the 8 simple steps outlined in my fluoride detox guide.
The basics are this, stop adding fuel to the fire (eliminate fluoride exposure) followed by detoxing your body of the fluoride it has accumulated over the years.
See you there!
- Jack CR Jr, Knopman DS, Jagust WJ, Shaw LM, Aisen PS, Weiner MW, Petersen RC, Trojanowski JQ. Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurol. 2010;9:119–28.
- Bhat SA, Kamal MA, Yarla NS, Ashraf GM. Synopsis on Management strategies for neurodegenerative disorders: challenges from bench to bedside in successful drug discovery and development. Curr Top Med Chem. 2017;17:1371–8.
- Livingston G, Sommerlad A, Orgeta V, Costafreda SG, Huntley J, Ames D, Ballard C, Banerjee S, Burns A, Cohen-Mansfield J, et al. Dementia prevention, intervention, and care. Lancet. 2017;390:2673–734.
- 4.Campdelacreu, J. Parkinson’s disease and Alzheimer disease: Environmental risk factors. Neurologia 2014, 29, 541–549.
- Sharma D, Singh A, Verma K, Paliwal S, Sharma S, Dwivedi J. Fluoride: a review of pre-clinical and clinical studies. Environ Toxicol Phar. 2016;56:297–313.
- Valdez-Jiménez L, Soria Fregozo C, Miranda Beltrán ML, Gutiérrez Coronado O, Pérez Vega MI. Effects of the fluoride on the central nervous system. Neurologia. 2011;26(5):297–300.
- Yan N, Liu Y, Liu S, Cao S, Wang F, Wang Z, et al. Fluoride-induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain. Mol Neurobiol. 2016;53(7):4449–60.
- Gutowska, I.; Baranowska-Bosiacka, I.; Goschorska, M.; Kolasa, A.; Łukomska, A.; Jakubczyk, K.; Dec, K.; Chlubek, D. Fluoride as a factor initiating and potentiating inflammation in monocytes/macrophages. Toxicol. In Vitro 2015, 29, 1661–1668.
- Cynthia G. Wible. Hippocampal Physiology, Structure and Function. Behav Sci (Basel). 2013 Jun; 3(2): 298–315.
- Kunz D, Schmitz S, Mahlberg R, Mohr A, Stoter C, Wolf KJ, Herrmann WM. A new concept for melatonin deficit: on pineal calcification and melatonin excretion. Neuropsychopharmacology, (6):765-772
- Bumb JM, Brockmann MA, Groden C, Nolte I. Microstructural analysis of pineal volume using trueFISP imaging. World J Radiol. 2013;5:166–72.
- Bumb JM, Schilling C, Enning F, Haddad L, Paul F, Lederbogen F, Deuschle M, Schredl M, Nolte I. Pineal gland volume in primary insomnia and healthy controls: a magnetic resonance imaging study. J Sleep Res. 2014;23:274–80.
- Turgut AT, Karakas HM, Ozsunar Y, Altin L, Ceken K, Alicioglu B, Sonmez I, Alparslan A, Yurumez B, Celik T, et al. Age-related changes in the incidence of pineal gland calcification in Turkey: a prospective multicenter CT study. Pathophysiology. 2008;15:41–8.
- Mahlberg R, Walther S, Kalus P, Bohner G, Haedel S, Reischies FM, Kuhl KP, Hellweg R, Kunz D. Pineal calcification in Alzheimer’s disease: an in vivo study using computed tomography. Neurobiol Aging. 2008;29:203–9.
- Friedland RP, Luxenberg JS, Koss E. A quantitative study of intracranial calcification in dementia of the Alzheimer type. Int Psychogeriatr. 1990;2:36–43.
- Rosales-Corral SA, Acuna-Castroviejo D, Coto-Montes A, Boga JA, Manchester LC, Fuentes-Broto L, Korkmaz A, Ma S, Tan DX, Reiter RJ. Alzheimer’s disease: pathological mechanisms and the beneficial role of melatonin. J Pineal Res. 2012;52:167–202.
- He H, Dong W, Huang F. Anti-amyloidogenic and anti-apoptotic role of melatonin in Alzheimer disease. Curr Neuropharmacol. 2010;8:211–7.
- Tan DX, Manchester LC, Terron MP, Flores LJ, Reiter RJ. One molecule, many derivatives: a never-ending interaction of melatonin with reactive oxygen and nitrogen species? J Pineal Res. 2007;42:28–42.
- Song, J. Pineal gland dysfunction in Alzheimer’s disease: relationship with the immune-pineal axis, sleep disturbance, and neurogenesis. Mol Neurodegeneration 14, 28 (2019).
- Wu YH, Swaab DF. The human pineal gland and melatonin in aging and Alzheimer’s disease. J Pineal Res. 2005;38:145–52.
- Srinivasan V, Kaur C, Pandi-Perumal S, Brown GM, Cardinali DP. Melatonin and its agonist ramelteon in Alzheimer’s disease: possible therapeutic value. Int J Alzheimers Dis. 2010;2011:741974.
- Guarnieri B, Adorni F, Musicco M, Appollonio I, Bonanni E, Caffarra P, Caltagirone C, Cerroni G, Concari L, Cosentino FI, et al. Prevalence of sleep disturbances in mild cognitive impairment and dementing disorders: a multicenter Italian clinical cross-sectional study on 431 patients. Dement Geriatr Cogn Disord. 2012;33:50–8
- Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation. Biol Psychiatry. 2016;80:40–52.
- Irwin MR, Opp MR. Sleep health: reciprocal regulation of sleep and innate immunity. Neuropsychopharmacology. 2017;42:129–55.
- Cheignon C, Tomas M, Bonnefontrousselot D, Faller P, Hureau C, Collin F. Oxidative stress and the amyloid beta peptide in Alzheimer’s disease. Redox Biol. 2018;14:450–64.
- Rojasgutierrez E, Muñozarenas G, Treviño S Espinosa B, Chavez R, Rojas K, et al. Alzheimer’s disease and metabolic syndrome: a link from oxidative stress and inflammation to neurodegeneration.
- Chen Z, Zhong C. Oxidative stress in Alzheimer’s disease. Neurosci Bull. 2014;30:271–81.
- Gao Q, Liu YJ, Guan ZZ. Decreased learning and memory ability in rats with fluorosis: increased oxidative stress and reduced cholinesterase activity in the brain. Fluoride. 2009;42(4):277–85.
- Dong YT, Wang Y, Wei N, Zhang QF, Guan ZZ. Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors. Arch Toxicol. 2015;89(11):1981–91.