7 Ways Cannabis Can Protect The Brain


Cannabis kills brain cells, right? Think again…

It’s true, most of us can think of at least one committed stoner with a memory of a goldfish and a vacant, thousand yard stare. So it may seem counter-intuitive to suggest that the cannabis plant can actually protect the brain and prevent certain neurodegenerative diseases like Alzheimer’s from forming.

And yet, even though the US government officially denies any such therapeutic use of cannabis, it has taken out a patent on cannabinoids saying they ‘are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia’.

So, instead of damaging memory it would seem that cannabis could actually do quite the opposite, and even protect against age related memory loss and dementia.

 7-surprising-ways-cannabis-can-protect-the-brain

The Endocannabinoid System (ECS) – a therapeutic target:

Scientists have known for some time that the body’s Endocannabinoid System – the complex network of chemical compounds and receptors found throughout the central nervous (CB1) and the immune system (CB2) – is directly involved in the mechanisms of diseases like Alzheimer’s and Parkinson’s.  An increased CB2 expression (1) found in post-mortem brains Alzheimer’s patients has been thought to be the ECS’s attempt to counteract the chronic inflammation found in the disease, while in another study (2) on Alzheimer’s patients, reduced levels of the endocannabinoid anandamide were found, although conversely were elevated in Parkinson’s disease (3).

Researchers believe then that by targeting the Endocannabinoid system, therapeutic answers can be found for many of the neurodegenerative diseases affecting people in the 21st century. And much research is being carried out into how phytocannabinoids like THC and CBD can not only treat disease progression, but also even prevent certain neurodegenerative disorders from happening.

So why exactly is cannabis being posited as the brain protector of the future?

1. Cannabis protects the brain by reducing inflammation

It’s commonly held that chronic inflammation is at the root of many illnesses, including Alzheimer’s. Although it still remains unclear whether inflammation is a by product or a direct contributing factor, bringing an excessive inflammatory response into balance again, is generally believed to be of benefit.

Gary Wenk, PhD, professor of neuroscience, immunology and medical genetics at Ohio State University, has studied how to combat brain inflammation for over 25 years. He says, ‘PET imaging studies of humans have shown that after age thirty the brain gradually displays increasing evidence of inflammation. With advancing age, brain inflammation continues to worsen leading to a decline in the production of new neurons, called neurogenesis, that are important for making new memories’.

He coined the phrase ‘one puff is enough’ after suggesting that ingesting small amounts of cannabis over years can be enough to protect the brain against inflammation, saying ‘the evidence available from studies of humans and animal models of Alzheimer’s disease do indicate that long-term, low-dose daily exposure, during mid-life, to the complex blend of compounds found in the marijuana plant can effectively slow the brain processes underlying Alzheimer’s disease’.

2. Cannabis is a powerful antioxidant protecting against toxic build up in the brain

As well as patenting Cannabinoids as neuroprotectants, the US government also named them antioxidants. But the two qualities are indelibly linked.

An ageing brain has a tendency to accumulate excessive levels of glutamate, a neurotransmitter that is involved with nerve cell signalling. This can lead to glutamate toxicity, an overstimulation of the cell and ultimately cell death. When glutamate causes cellular damage, it becomes an excitotoxin. Excitotoxicity is viewed as a potential cause of many neurodegenerative diseases of the central nervous system, as well as strokes and hearing loss.

In one study (4) carried out on rats, the cannabinoid Cannabidiol was ‘was demonstrated to reduce hydroperoxide toxicity in neurons. In a head to head trial of the abilities of various antioxidants to prevent glutamate toxicity, cannabidiol was superior to both alpha-tocopherol and ascorbate in protective capacity.’  And in another, (5) THC was shown to reduce the levels of glutamate in the brain following a traumatic brain injury.

An additional age related toxicity that researchers believe may bring about the onset of diseases like Alzheimer’s and Parkinson’s is excessive levels of iron in the body.

Researchers from Pontifical Catholic University in Brazil (6) examined the relationship between high levels of iron and cell death in neurodegenerative diseases. In particular they studied the potential use of CBD, which they found may protect the rapid cell death associated with iron.

3. Cannabis helps promote new brain cell growth

7-ways-cannabis-can-protect-the-brain-1This is the one that really stops people in their tracks. Surely cannabis kills off brain cells, right? While it’s true in young, adolescent brains, cannabis can have a negative effect on brain development, scientists do know that the Endocannabinoid system is closely linked with the process of adult neurogenesis (brain cell growth).

Once again mice were the subjects of research (7) that showed the administration of plant cannabinoids promoted hippocampal neurogenesis – new cell growth in the region of the brain associated both with memory and learning – but also depression and anxiety.

In a follow on study (8) by the University of Saskatchewan, researchers sought to find out whether this hippocampal neurogenesis could explain the apparent anti anxiety and antidepressant effects of cannabinoids. Using a synthetic cannabinoid called HU-210 on rats, they found it gave rise to both the growth of ‘newborn neurons’ in the hippocampal area but also reduced anxiety and depression like behaviour in the animal subjects.

Thus showing that ‘cannabinoids appear to be the only illicit drug whose capacity to produce increased hippocampal newborn neurons is positively correlated with its anxiolytic- and antidepressant-like effects’.

4. Cannabis may slow the progression of some neurodegenerative diseases

We’ve seen that cannabis can potentially be a neuroprotector, but what effect does it have on slowing the progress of illnesses related to the brain and central nervous system?

So far, as generally is the case with research into the use of cannabis to treat disease, most findings are at the pre-clinical stage on animal models, or in the laboratory.

One such trial (9) has shown how CBD can reduce neural inflammation in mice injected with amyloid-beta, the protein that scientists believe leads to neuronal cell death in Alzheimer’s.

Research (10) carried out in 2014 at the University of South Florida showed that extremely low doses of THC actually reduces amyloid-beta production. “THC is known to be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer’s pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function,” said study lead author Chuanhai Cao, PhD of the study.

By increasing mitochondrial function it also means a healthier brain due to a better energy supply and improved signalling.

5. Cannabis can make Alzheimer’s patients less agitated

A small amount of clinical trials have taken place on Alzheimer’s patients using cannabinoids to lessen levels of agitation.

One double-blind, placebo-controlled, six-week, crossover study of 12 patients suffering from Alzheimer-type dementia reported that 5 mg of dronabinol (delta 9-THC) daily was associated with a decrease in disturbed behaviour (11).

 A recent study (12) carried out on 11 patients in Israel found that out of the 10 patients that completed the trial ingesting medical cannabis oil, researchers recorded “significant reduction” in behavioural and psychological symptoms of dementia. Researchers concluded that ‘adding medical cannabis oil  to Alzheimer’s patients’ pharmacotherapy is safe and a promising treatment option’.

6. Cannabis may protect the brain against serious brain trauma

5.3 million people live with traumatic brain injury (TBI) in the US, a number comparable to those living with Alzheimer’s. It is caused by a severe blow to the head and resulting symptoms can include cognitive problems such as headache, difficulty thinking, memory problems, attention deficits, mood swings and frustration.

TBI is also proving an exciting area of research for the potential therapeutic use of cannabinoids. THC in particular has been shown to protect the brain from long term damage following a traumatic injury. In a study (13) carried out on mice by Professor Yosef Sarne of Tel Aviv University, very low doses of THC administered over a long period of time were found to ‘protect the brain from long-term cognitive damage in the wake of injury from hypoxia (lack of oxygen), seizures, or toxic drugs’.

Not only did they find that THC minimised the damage to the brain following an injury, but if administered before the incident it could prevent brain injury from occurring in the first place. It seems strange to suggest taking THC just in case a brain trauma might occur, but in instances such as major surgery when blood supply to the brain is interrupted, THC’s neuroprotection could be of benefit.

This theory appears to be backed up by a study (14) carried out at a hospital in California reviewing the data of 446 adults treated for brain injuries. Overall 1 in 5 patients tested positive for THC and compared to the patients who hadn’t tested positive, they were statistically 80% less likely to die from their injuries.

While this doesn’t demonstrate a direct cause and effect between THC use and survival from serious brain trauma, the findings certainly highlight the potential use of cannabinoids for giving the best chances of recovery.

7. Cannabis could limit brain damage resulting from strokes

7-ways-cannabis-can-protect-the-brain-strokeWhereas a TBI is caused by an external force injuring the brain, a stroke occurs when due to a thickening of the arteries, there is poor blood flow to the brain, resulting in cell death, partial paralysis etc.

Scientists are slowly beginning to realise how the endocannabinoid system is activated during a stroke (15) whereby ‘activation of the CB receptors leads to cellular changes that are extremely relevant to ischemic injury (stroke damage): they regulate glutamate release, nitric oxide synthesis, growth factor expression, cellular antioxidant activity, the release of inflammatory cytokines, and leukocyte adhesion to cerebral vessels.’

Both CBD and THC’s ability to block the neurotransmitter glutamate, produced when the brain is deprived of oxygen, once again come to the fore as a way to limit cell death following a stroke. In a study (16) published in 2010 scientists concluded that ‘CBD had a potent and long-lasting neuroprotective effect and prevented progressive post-ischemic injury’ and ‘that repeated treatment with CBD from 1 day or 3 days after cerebral ischemia improved the functional deficits, such as neurological score and motor coordination, and survival rates’.

Another rodent study (17) showed Cannabidiol to have ‘a protective effect on neuronal death induced by ischemia (stroke)’ indicating that it ‘might exert beneficial therapeutic effects in brain ischemia’.

So contrary to the commonly held belief that cannabis leads to the loss of precious neurones, studies increasingly show the potential benefits for protecting our ageing brains against neurodegeneration and even injury from external forces.

It’s clear that there is a lot still to understand about the endocannabinoid system’s role in these particular diseases, but scientists remain hopeful that the many theories honed in the lab may one day move forward into the realms of clinical trials, and eventually to treatment for patients.

References:

  1. Solas M1, Francis PT, Franco R, Ramirez MJ (2013). CB2 receptor and amyloid pathology in frontal cortex of Alzheimer’s disease patients. Neurobiol Aging. 2013 Mar;34(3):805-8.
  2. Kwang-Mook Jung,a,1 Giuseppe Astarita,a,1 Sevil Yasar,d Vitaly Vasilevko,c David H. Cribbs,c Elizabeth Head,c,2 Carl W. Cotman,c and Daniele Piomelli (2012). An amyloid beta 42-dependent deficit in anandamide mobilization is associated with cognitive dysfunction in Alzheimer’s disease.Neurobiol Aging 2012 Aug; 33(8): 1522–1532.
  3. Pisani V1, Moschella V, Bari M, Fezza F, Galati S, Bernardi G, Stanzione P, Pisani A, Maccarrone M. (2010) Dynamic changes of anandamide in the cerebrospinal fluid of Parkinson’s disease patients. Movement Disorders.15;25(7):920-4.
  4. Hampson AJ1, Grimaldi M, Lolic M, Wink D, Rosenthal R, Axelrod J.(2000) Neuroprotective antioxidants from marijuana. Annals of the New York Academy of Sciences 899:274-82.
  5. Esther Shohami, Ayelet Cohen-Yeshurun, Lital Magid, Merav Algali, and Raphael Mechoulam (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology.  163(7): 1402–1410
  6. Vanessa Kappel da Silva, Betânia Souza de Freitas, Arethuza da Silva Dornelles,Laura Roesler Nery, Lucio Falavigna,Rafael Dal Ponte Ferreira, Maurício Reis Bogo, Jaime Eduardo Cecílio Hallak, Antônio Waldo Zuardi, José Alexandre S. Crippa, Nadja Schröder (2014) Cannabidiol Normalizes Caspase 3, Synaptophysin, and Mitochondrial Fission Protein DNM1L Expression Levels in Rats with Brain Iron Overload: Implications for Neuroprotection. Molecular Neurobiology. Volume 49, Issue 1, pp 222–233
  7. Jin K1, Xie L, Kim SH, Parmentier-Batteur S, Sun Y, Mao XO, Childs J, Greenberg DA. (2004) Defective adult neurogenesis in CB1 cannabinoid receptor knockout mice. Molecular Pharmacology. 66(2):204-8.
  8. Jiang W1, Zhang Y, Xiao L, Van Cleemput J, Ji SP, Bai G, Zhang X (2005). Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.The Journal of Clinical Investigation. (11):3104-16.
  9. G Esposito, C Scuderi, C Savani, L Steardo, Jr, D De Filippis, P Cottone, T Iuvone, V Cuomo, and L Steardo (2007). Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1? and iNOS expression. British Journal of Pharmacology. 151(8): 1272–1279
  10. Cao C, Li Y, Liu H, Bai G, Mayl J, Lin X, Sutherland K, Nabar N, Cai J. (2014) The potential therapeutic effects of THC on Alzheimer’s disease. Journal of Alzheimer’s Disease 42(3):973-84
  11. Volicer, L., Stelly, M., Morris, J., McLaughlin, J. and others. (1997). Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer’s disease. Int.J.Geriatr.Psychiatry. 12: 913-919.
  12. Shelef A, Barak Y, Berger U, Paleacu D, Tadger S, Plopsky I, Baruch Y. (2016) Safety and Efficacy of Medical Cannabis Oil for Behavioral and Psychological Symptoms of Dementia: An-Open Label, Add-On, Pilot Study. Journal of Alzheimer’s Disease. 51(1):15-9
  13. Fishbein M, Gov S, Assaf F, Gafni M, Keren O, Sarne Y. ( 2012) Long-term behavioral and biochemical effects of an ultra-low dose of delta 9-tetrahydrocannabinol (THC): neuroprotection and ERK signaling. Experimental Brain Research. 221(4):437-48
  14. Nguyen BM, Kim D, Bricker S, Bongard F, Neville A, Putnam B, Smith J, Plurad D. (2014) Effect of marijuana use on outcomes in traumatic brain injury. American Surgeon. Oct;80(10):979-83.
  15. Cecilia J. Hillard (2008) Role of cannabinoids and endocannabinoids in cerebral ischemia. Current Pharmaceutical Design 14(23): 2347–2361.
  16. Kazuhide Hayakawa, Kenichi Mishima, and Michihiro Fujiwara (2010). Therapeutic Potential of Non-Psychotropic Cannabidiol in Ischemic Stroke. Pharmaceuticals 3(7): 2197–2212.
  17. Schiavon AP, Soares LM, Bonato JM, Milani H, Guimarães FS, Weffort de Oliveira RM.(2014) Protective effects of cannabidiol against hippocampal cell death and cognitive impairment induced by bilateral common carotid artery occlusion in mice. Neurotoxicity Research 26(4):307-16

Source:https://wakeup-world.com

7 Ways Cannabis Can Protect The Brain.


Cannabis kills brain cells, right? Think again…

It’s true, most of us can think of at least one committed stoner with a memory of a goldfish and a vacant, thousand yard stare. So it may seem counter-intuitive to suggest that the cannabis plant can actually protect the brain and prevent certain neurodegenerative diseases like Alzheimer’s from forming.

And yet, even though the US government officially denies any such therapeutic use of cannabis, it has taken out a patent on cannabinoids saying they ‘are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia’.

So, instead of damaging memory it would seem that cannabis could actually do quite the opposite, and even protect against age related memory loss and dementia.

The Endocannabinoid System (ECS) – a therapeutic target:

Scientists have known for some time that the body’s Endocannabinoid System – the complex network of chemical compounds and receptors found throughout the central nervous (CB1) and the immune system (CB2) – is directly involved in the mechanisms of diseases like Alzheimer’s and Parkinson’s.  An increased CB2 expression (1) found in post-mortem brains Alzheimer’s patients has been thought to be the ECS’s attempt to counteract the chronic inflammation found in the disease, while in another study (2) on Alzheimer’s patients, reduced levels of the endocannabinoid anandamide were found, although conversely were elevated in Parkinson’s disease (3).

Researchers believe then that by targeting the Endocannabinoid system, therapeutic answers can be found for many of the neurodegenerative diseases affecting people in the 21st century. And much research is being carried out into how phytocannabinoids like THC and CBD can not only treat disease progression, but also even prevent certain neurodegenerative disorders from happening.

So why exactly is cannabis being posited as the brain protector of the future?

1. Cannabis protects the brain by reducing inflammation

It’s commonly held that chronic inflammation is at the root of many illnesses, including Alzheimer’s. Although it still remains unclear whether inflammation is a by product or a direct contributing factor, bringing an excessive inflammatory response into balance again, is generally believed to be of benefit.

Gary Wenk, PhD, professor of neuroscience, immunology and medical genetics at Ohio State University, has studied how to combat brain inflammation for over 25 years. He says, ‘PET imaging studies of humans have shown that after age thirty the brain gradually displays increasing evidence of inflammation. With advancing age, brain inflammation continues to worsen leading to a decline in the production of new neurons, called neurogenesis, that are important for making new memories’.

He coined the phrase ‘one puff is enough’ after suggesting that ingesting small amounts of cannabis over years can be enough to protect the brain against inflammation, saying ‘the evidence available from studies of humans and animal models of Alzheimer’s disease do indicate that long-term, low-dose daily exposure, during mid-life, to the complex blend of compounds found in the marijuana plant can effectively slow the brain processes underlying Alzheimer’s disease’.

2. Cannabis is a powerful antioxidant protecting against toxic build up in the brain

As well as patenting Cannabinoids as neuroprotectants, the US government also named them antioxidants. But the two qualities are indelibly linked.

An ageing brain has a tendency to accumulate excessive levels of glutamate, a neurotransmitter that is involved with nerve cell signalling. This can lead to glutamate toxicity, an overstimulation of the cell and ultimately cell death. When glutamate causes cellular damage, it becomes an excitotoxin. Excitotoxicity is viewed as a potential cause of many neurodegenerative diseases of the central nervous system, as well as strokes and hearing loss.

In one study (4) carried out on rats, the cannabinoid Cannabidiol was ‘was demonstrated to reduce hydroperoxide toxicity in neurons. In a head to head trial of the abilities of various antioxidants to prevent glutamate toxicity, cannabidiol was superior to both alpha-tocopherol and ascorbate in protective capacity.’  And in another, (5) THC was shown to reduce the levels of glutamate in the brain following a traumatic brain injury.

An additional age related toxicity that researchers believe may bring about the onset of diseases like Alzheimer’s and Parkinson’s is excessive levels of iron in the body.

Researchers from Pontifical Catholic University in Brazil (6) examined the relationship between high levels of iron and cell death in neurodegenerative diseases. In particular they studied the potential use of CBD, which they found may protect the rapid cell death associated with iron.

3. Cannabis helps promote new brain cell growth

7-ways-cannabis-can-protect-the-brain-1This is the one that really stops people in their tracks. Surely cannabis kills off brain cells, right? While it’s true in young, adolescent brains, cannabis can have a negative effect on brain development, scientists do know that the Endocannabinoid system is closely linked with the process of adult neurogenesis (brain cell growth).

Once again mice were the subjects of research (7) that showed the administration of plant cannabinoids promoted hippocampal neurogenesis – new cell growth in the region of the brain associated both with memory and learning – but also depression and anxiety.

In a follow on study (8) by the University of Saskatchewan, researchers sought to find out whether this hippocampal neurogenesis could explain the apparent anti anxiety and antidepressant effects of cannabinoids. Using a synthetic cannabinoid called HU-210 on rats, they found it gave rise to both the growth of ‘newborn neurons’ in the hippocampal area but also reduced anxiety and depression like behaviour in the animal subjects.

Thus showing that ‘cannabinoids appear to be the only illicit drug whose capacity to produce increased hippocampal newborn neurons is positively correlated with its anxiolytic- and antidepressant-like effects’.

4. Cannabis may slow the progression of some neurodegenerative diseases

We’ve seen that cannabis can potentially be a neuroprotector, but what effect does it have on slowing the progress of illnesses related to the brain and central nervous system?

So far, as generally is the case with research into the use of cannabis to treat disease, most findings are at the pre-clinical stage on animal models, or in the laboratory.

One such trial (9) has shown how CBD can reduce neural inflammation in mice injected with amyloid-beta, the protein that scientists believe leads to neuronal cell death in Alzheimer’s.

Research (10) carried out in 2014 at the University of South Florida showed that extremely low doses of THC actually reduces amyloid-beta production. “THC is known to be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer’s pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function,” said study lead author Chuanhai Cao, PhD of the study.

By increasing mitochondrial function it also means a healthier brain due to a better energy supply and improved signalling.

5. Cannabis can make Alzheimer’s patients less agitated

A small amount of clinical trials have taken place on Alzheimer’s patients using cannabinoids to lessen levels of agitation.

One double-blind, placebo-controlled, six-week, crossover study of 12 patients suffering from Alzheimer-type dementia reported that 5 mg of dronabinol (delta 9-THC) daily was associated with a decrease in disturbed behaviour (11).

A recent study (12) carried out on 11 patients in Israel found that out of the 10 patients that completed the trial ingesting medical cannabis oil, researchers recorded “significant reduction” in behavioural and psychological symptoms of dementia. Researchers concluded that ‘adding medical cannabis oil  to Alzheimer’s patients’ pharmacotherapy is safe and a promising treatment option’.

6. Cannabis may protect the brain against serious brain trauma

5.3 million people live with traumatic brain injury (TBI) in the US, a number comparable to those living with Alzheimer’s. It is caused by a severe blow to the head and resulting symptoms can include cognitive problems such as headache, difficulty thinking, memory problems, attention deficits, mood swings and frustration.

TBI is also proving an exciting area of research for the potential therapeutic use of cannabinoids. THC in particular has been shown to protect the brain from long term damage following a traumatic injury. In a study (13) carried out on mice by Professor Yosef Sarne of Tel Aviv University, very low doses of THC administered over a long period of time were found to ‘protect the brain from long-term cognitive damage in the wake of injury from hypoxia (lack of oxygen), seizures, or toxic drugs’.

Not only did they find that THC minimised the damage to the brain following an injury, but if administered before the incident it could prevent brain injury from occurring in the first place. It seems strange to suggest taking THC just in case a brain trauma might occur, but in instances such as major surgery when blood supply to the brain is interrupted, THC’s neuroprotection could be of benefit.

This theory appears to be backed up by a study (14) carried out at a hospital in California reviewing the data of 446 adults treated for brain injuries. Overall 1 in 5 patients tested positive for THC and compared to the patients who hadn’t tested positive, they were statistically 80% less likely to die from their injuries.

While this doesn’t demonstrate a direct cause and effect between THC use and survival from serious brain trauma, the findings certainly highlight the potential use of cannabinoids for giving the best chances of recovery.

7. Cannabis could limit brain damage resulting from strokes

7-ways-cannabis-can-protect-the-brain-strokeWhereas a TBI is caused by an external force injuring the brain, a stroke occurs when due to a thickening of the arteries, there is poor blood flow to the brain, resulting in cell death, partial paralysis etc.

Scientists are slowly beginning to realise how the endocannabinoid system is activated during a stroke (15) whereby ‘activation of the CB receptors leads to cellular changes that are extremely relevant to ischemic injury (stroke damage): they regulate glutamate release, nitric oxide synthesis, growth factor expression, cellular antioxidant activity, the release of inflammatory cytokines, and leukocyte adhesion to cerebral vessels.’

Both CBD and THC’s ability to block the neurotransmitter glutamate, produced when the brain is deprived of oxygen, once again come to the fore as a way to limit cell death following a stroke. In a study (16) published in 2010 scientists concluded that ‘CBD had a potent and long-lasting neuroprotective effect and prevented progressive post-ischemic injury’ and ‘that repeated treatment with CBD from 1 day or 3 days after cerebral ischemia improved the functional deficits, such as neurological score and motor coordination, and survival rates’.

Another rodent study (17) showed Cannabidiol to have ‘a protective effect on neuronal death induced by ischemia (stroke)’ indicating that it ‘might exert beneficial therapeutic effects in brain ischemia’.

So contrary to the commonly held belief that cannabis leads to the loss of precious neurones, studies increasingly show the potential benefits for protecting our ageing brains against neurodegeneration and even injury from external forces.

It’s clear that there is a lot still to understand about the endocannabinoid system’s role in these particular diseases, but scientists remain hopeful that the many theories honed in the lab may one day move forward into the realms of clinical trials, and eventually to treatment for patients.

References:

  1. Solas M1, Francis PT, Franco R, Ramirez MJ (2013). CB2 receptor and amyloid pathology in frontal cortex of Alzheimer’s disease patients. Neurobiol Aging. 2013 Mar;34(3):805-8.
  2. Kwang-Mook Jung,a,1 Giuseppe Astarita,a,1 Sevil Yasar,d Vitaly Vasilevko,c David H. Cribbs,c Elizabeth Head,c,2 Carl W. Cotman,c and Daniele Piomelli (2012). An amyloid beta 42-dependent deficit in anandamide mobilization is associated with cognitive dysfunction in Alzheimer’s disease.Neurobiol Aging 2012 Aug; 33(8): 1522–1532.
  3. Pisani V1, Moschella V, Bari M, Fezza F, Galati S, Bernardi G, Stanzione P, Pisani A, Maccarrone M. (2010) Dynamic changes of anandamide in the cerebrospinal fluid of Parkinson’s disease patients. Movement Disorders.15;25(7):920-4.
  4. Hampson AJ1, Grimaldi M, Lolic M, Wink D, Rosenthal R, Axelrod J.(2000) Neuroprotective antioxidants from marijuana. Annals of the New York Academy of Sciences 899:274-82.
  5. Esther Shohami, Ayelet Cohen-Yeshurun, Lital Magid, Merav Algali, and Raphael Mechoulam (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology.  163(7): 1402–1410
  6. Vanessa Kappel da Silva, Betânia Souza de Freitas, Arethuza da Silva Dornelles,Laura Roesler Nery, Lucio Falavigna,Rafael Dal Ponte Ferreira, Maurício Reis Bogo, Jaime Eduardo Cecílio Hallak, Antônio Waldo Zuardi, José Alexandre S. Crippa, Nadja Schröder (2014) Cannabidiol Normalizes Caspase 3, Synaptophysin, and Mitochondrial Fission Protein DNM1L Expression Levels in Rats with Brain Iron Overload: Implications for Neuroprotection. Molecular Neurobiology. Volume 49, Issue 1, pp 222–233
  7. Jin K1, Xie L, Kim SH, Parmentier-Batteur S, Sun Y, Mao XO, Childs J, Greenberg DA. (2004) Defective adult neurogenesis in CB1 cannabinoid receptor knockout mice. Molecular Pharmacology. 66(2):204-8.
  8. Jiang W1, Zhang Y, Xiao L, Van Cleemput J, Ji SP, Bai G, Zhang X (2005). Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.The Journal of Clinical Investigation. (11):3104-16.
  9. G Esposito, C Scuderi, C Savani, L Steardo, Jr, D De Filippis, P Cottone, T Iuvone, V Cuomo, and L Steardo (2007). Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1? and iNOS expression. British Journal of Pharmacology. 151(8): 1272–1279
  10. Cao C, Li Y, Liu H, Bai G, Mayl J, Lin X, Sutherland K, Nabar N, Cai J. (2014) The potential therapeutic effects of THC on Alzheimer’s disease. Journal of Alzheimer’s Disease 42(3):973-84
  11. Volicer, L., Stelly, M., Morris, J., McLaughlin, J. and others. (1997). Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer’s disease. Int.J.Geriatr.Psychiatry. 12: 913-919.
  12. Shelef A, Barak Y, Berger U, Paleacu D, Tadger S, Plopsky I, Baruch Y. (2016) Safety and Efficacy of Medical Cannabis Oil for Behavioral and Psychological Symptoms of Dementia: An-Open Label, Add-On, Pilot Study. Journal of Alzheimer’s Disease. 51(1):15-9
  13. Fishbein M, Gov S, Assaf F, Gafni M, Keren O, Sarne Y. ( 2012) Long-term behavioral and biochemical effects of an ultra-low dose of delta 9-tetrahydrocannabinol (THC): neuroprotection and ERK signaling. Experimental Brain Research. 221(4):437-48
  14. Nguyen BM, Kim D, Bricker S, Bongard F, Neville A, Putnam B, Smith J, Plurad D. (2014) Effect of marijuana use on outcomes in traumatic brain injury. American Surgeon. Oct;80(10):979-83.
  15. Cecilia J. Hillard (2008) Role of cannabinoids and endocannabinoids in cerebral ischemia. Current Pharmaceutical Design 14(23): 2347–2361.
  16. Kazuhide Hayakawa, Kenichi Mishima, and Michihiro Fujiwara (2010). Therapeutic Potential of Non-Psychotropic Cannabidiol in Ischemic Stroke. Pharmaceuticals 3(7): 2197–2212.
  17. Schiavon AP, Soares LM, Bonato JM, Milani H, Guimarães FS, Weffort de Oliveira RM.(2014) Protective effects of cannabidiol against hippocampal cell death and cognitive impairment induced by bilateral common carotid artery occlusion in mice. Neurotoxicity Research 26(4):307-16

Source:https://wakeup-world.com

How Intermittent Fasting Can Slow Degenerative Disease, Protect the Brain and Slim the Body


“Humans live on one-quarter of what they eat; on the other three-quarters lives their doctor.” ~ Egyptian pyramid inscription, 3800 B.C.

Mark Mattson is an expert on food deprivation. A scientist at the National Institute on Aging and a professor of neuroscience at Johns Hopkins School of Medicine, Mattson has been studying for decades the effect fasting has on mental and physical health, as well as how it influences aging. He’s considered the foremost expert in the field of Alzheimer’s and brain research. And he’s a major advocate for skipping meals.

Mattson himself only eats one meal a day — and says, because of it, he has more energy, mental clarity and focus, along with heightened levels of productivity. “As is similar to what happens when muscles are exercised, the neurons in the brain benefit from being mildly stressed. To achieve the right kind of stress, people might benefit from severely minimizing their food intake,” he told Michael Anft in “Don’t feed your head.” Worldwide, participants involved with various forms of fasting have healed a wide-range of health complaints, from diabetes to obesity and heart disease.

Now a number of physicians have come forward, enthusiastically praising the benefits of the practice. But in the West, where access to food is abundant and even excessive, the thought of going without appears to be a ghastly and unpleasant exercise in unnecessary hardship. Even so, when faced with sky-rocketing cancer rates and an uncomfortable spike in Alzheimer’s disease, our curiosity might just get the better of us — and we may decide to have a look at this seemingly foreign practice, which promises exceptional health and more.

Why fast?

When we explore how our bodies evolved, fasting makes quite a bit of sense on several levels. Obviously, grocery stores and access to food 24/7 isn’t how we developed as humans. A more realistic scenario encompasses food scarcity — especially during seasons of severe weather. Winter and spring are traditionally lean times, where our bodies naturally adapt to lower caloric intake. Part of this adaptation involves the brain, as Mattson explains:

“Our ancestors undoubtedly had to go without food for stretches of time. It hasn’t been that long since humanity lacked regular supplies of food. When you search for food when you’re hungry, the brain is really engaged. The individuals who survive the best—the ones whose brains are more attuned to predators and who can remember where food sources are—are the ones who’ve survived.”

When we fast, messaging chemicals that operate at the cellular level are stimulated, which encourage the growth of brain cells. As these neurons grow, a protective mechanism kicks in and our brain becomes more resistant to damage caused by Parkinson’s, or the protein plaques that aggravate cases of Alzheimer’s.

It has long been known that fasting exerts a positive influence over those who suffer from epileptic seizures. Scientists believe calorie deprivation triggers a process within the brain that helps to calm the overexcited signals which an epileptic brain displays. Overfed normal brains exhibit another kind of unruly excitation, which ultimately leads to impairment in brain function.

Ketones are also produced — a type of acid that is created when the body begins to use fat instead of carbohydrates for energy. In lieu of glucose, ketones provide an alternate, less damaging fuel for the brain. Fasting also increases the number of mitochondria in nerve cells, creating more energy in the process. Fasting improves learning and memory factors as well.

fasting

If improved brain function isn’t enough to convince you to give fasting a try, consider this: the practice can significantly lower the risk of cancer and heart disease — and even reverse early-stage diabetes.

How the “Fast Diet” can revolutionize health

Overweight and pre-diabetic, Dr. Michael Mosley decided to forgo the standard regiment of pharmaceuticals and instead seek a solution to his health issues elsewhere.

“I started off by looking at calorie restriction and saw that the research was really great — it’s pretty much the only thing that extends life,” Mosley told the Huffington Post. “The problem is it just is impossible to do — I could not imagine myself never eating the things I love. So I started investigating intermittent fasting as a way to control calories.”

Mosley spent months researching the science behind intermittent fasting — a method of drastically altering caloric intake — and eventually tested the approach on himself. As the experiment progressed over three months, he shed 19 pounds of fat and watched his cholesterol normalize. Moreover, his insulin resistance completely disappeared.

The version of fasting described in Mosley’s bestselling book — “The Fast Diet” — is one of the least uncomfortable forms of the practice. Called the 5:2 plan, it prescribes normal eating patterns for five days a week and then two days of fasting on less than 500 calories per day for women, 600 for men. According to the book, inflammation is curbed and degenerative disease is significantly slowed — if not completely prevented. A happy side-effect of the program is a svelte physique where fat — not muscle — is reduced. Additionally, animal tests have shown food restriction retards aging and increases longevity by an impressive 30-40%.

With all the benefits of fasting, why wouldn’t Westerners embrace the practice with open arms? Besides the usual aversion to even the slightest discomfort, Mark Mattson suspects another culprit behind our resistence, which he addresses in his TEDx Johns Hopkins University talk:

“There are a lot of pressures to have that eating pattern [three meals a day plus snacks]. There’s a lot of money involved. The food industry — are they going to make money from skipping breakfast like I did today? No, they’re going to lose money. If people fast, the food industry loses money. What about the pharmaceutical industries? What if people do intermittent fasting and exercise periodically and they are very healthy, is the pharmaceutical industry going to make any money on healthy people?”

There are several methods of intermittent fasting. Dr. Mercola provides another example with this infographic:

The Benefits of Intermittent Fasting - Mercola

Watch the video discussion. URL: https://youtu.be/cATFCKtJnwg