Education Linked to Brain Tumor Risk

Education and socioeconomic status have been linked with cancer outcomes, but a new study now links higher education with the development of certain types of cancer.

The large observational study, published in the Journal of Epidemiology and Community Health, reports that a high level of education is associated with an increased risk of brain tumors. The study is based on data from 4.3 million Swedish adults who were monitored between 1993 and 2010. Overall, 5,735 men and 7,101 women developed a brain tumor during the observation period.

Men with at least three years of university-level education had a 19% greater risk of developing gliomas than men with only a compulsory level of education (nine years). Women with the same level of education had a 23% increased risk of gliomas and a 16% increased risk of meningiomas. Marital status and amount of disposable income only slightly affected the risk among men but not among women. Single men had a lower risk of glioma but a higher risk of meningiomas. Occupation also influenced brain tumor risks among men and women: men in professional and management roles had a 20% increased risk of gliomas and a 50% increased risk of acoustic neuromas; women in these roles had a 26% increased risk of gliomas and a 14% increased risk of meningiomas.

Socioeconomic status has been associated with prognosis and outcomes in many types of cancer, as well as the development of breast cancer, childhood leukemia, and Hodgkin’s lymphoma. Socioeconomic status and education level also affect attitudes toward cancer screening and treatment and timeliness of disease presentation. Age, military service record, and insurance coverage have also been associated with cancer risks and outcomes. The reasons behind the associations are unclear, but some risk factors have been hypothesized such as rates of atopy and allergies, cell phone use, and body measurements.

While no firm cause-and-effect conclusions can be drawn from an observational study, the authors of the new study claim that the results are consistent and that examining a large population gives strength to the results. More evidence is needed to confirm if education is, in fact, a true risk factor for developing brain tumors.

References

Borugian MJ, Spinelli JJ, Mezei G, Wilkins R, Abanto Z, & McBride ML (2005). Childhood leukemia and socioeconomic status in Canada. Epidemiology (Cambridge, Mass.), 16 (4), 526-31 PMID: 15951671

Clarke CA, Glaser SL, Keegan TH, & Stroup A (2005). Neighborhood socioeconomic status and Hodgkin’s lymphoma incidence in California. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 14 (6), 1441-7 PMID: 15941953

Kasl RA, Brinson PR, & Chambless LB (2016). Socioeconomic status does not affect prognosis in patients with glioblastoma multiforme. Surgical neurology international, 7 (Suppl 11) PMID: 27217966

Lehrer S, Green S, & Rosenzweig KE (2016). Affluence and Breast Cancer. The breast journal PMID: 27296617

Mezei G, Borugian MJ, Spinelli JJ, Wilkins R, Abanto Z, & McBride ML (2006). Socioeconomic status and childhood solid tumor and lymphoma incidence in Canada. American journal of epidemiology, 164 (2), 170-5 PMID: 16524952

Porter AB, Lachance DH, & Johnson DR (2015). Socioeconomic status and glioblastoma risk: a population-based analysis. Cancer causes & control : CCC, 26 (2), 179-85 PMID: 25421378

Quaife SL, Winstanley K, Robb KA, Simon AE, Ramirez AJ, Forbes LJ, Brain KE, Gavin A, & Wardle J (2015). Socioeconomic inequalities in attitudes towards cancer: an international cancer benchmarking partnership study. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP), 24 (3), 253-60 PMID: 25734238

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Stop Procrastinating Before You Even Start using Emotional Control

For readers looking to jump into the deep end of understanding procrastination, I highly recommend the recent volume edited by James Gross, Handbook of Emotion Regulation. This collection of chapters provides the most current and thorough review of the research literature in the area. Because I have put such emphasis in my own writing on the role of emotions in understanding procrastination, I thought I would summarize aspects of just one of the many chapters of this excellent book. The reference to the chapter written by Dylan Wagner and Todd Heatherton is below.

I was amused and delighted by the metaphor and image that these authors used to depict the role of negative emotions (also called negative affect) in the self-regulation process. In a very typical, academic-style diagram of a model of self-regulation, they first depict a high-level theoretical perspective.

The essential components conceptually look something like this:

TEMPTATIONS & DESIRES    GOALS & STANDARDS    Success

(food, drugs, media use, etc.)    Monitoring Capacity        Failure

At the center of the model are our goals and standards. In other words, central to self-regulation is monitoring our progress towards our goals and our capacity to do this. What they depict as directly influencing our goals and standards are temptations and desires. You know, other more fun stuff. Finally, the model makes it clear that depending on how well we can ignore the temptations while maintaining our goal pursuit predicts whether we succeed or fail. In sum, it’s a common, simple model of self-regulation that is typical of a scholarly paper.

The amusing bit is how they chose to depict the effects of negative affect (negative emotions). They have the same diagram but with a giant black hole underneath the model out of which evil tendrils emerge. These tendrils, as tendrils will, grab on to every component of the model. This model now emphasizes a failure outcome, and the final piece of the model is how failure now feeds back down to the hole from which the tendrils emerge and feed the negative affect.

[Note: While I am tempted to add a photo of their diagram here, there are copyright laws that prevent usage in this way, so I hope that this description allowed you to imagine this quite vivid depiction of a psychological model.]

As they note in the caption to this figure:

“Negative affect spreads poison tendrils into every aspect of self-regulation, amplifying desires, decreasing monitoring, depleting limited capacity, and encouraging misregulation strategies [e.g., mood repair and escape from aversive self-awareness], which can relieve negative affect in the short term but often lead to further negative affect upon failure to meet one’s goals”

Well done! That’s certainly the lived experience of the effects of negative emotions on our self-regulation. The tendrils pull us down.

These negative emotions seem to emerge from a dark place within us, grabbing on to every aspect of our self, and undermine our ability to self-regulate. And, of course, as we fail in our attempts to self-regulate, the self-blame begins, as does the downward spiral of self-esteem and self-efficacy.

In the bulk of the chapter, Wagner and Heatherton summarize numerous studies related to the different ways that negative emotions, emotion regulation and self-regulation interact. It’s important to remember that these are interactive effects, or as I like to say, it’s a sort of dance between these processes that undermine our success. As the authors summarize this interaction, we learn the following:

• Negative affect (emotions) leads to a desire to “feel good now,” escaping the negative state by engaging in pleasurable activities and reducing self-awareness (to lower any potential feelings of guilt; a process I have described previously);
• These choices related to mood repair serve to increase the pull or attractiveness of immediately available rewards and temptations grow;
• With a focus on pleasure and lower self-awareness, the ability to self-monitor is diminished; and at the same time,
• Negative affect, which is related to rumination, puts an increased load on working memory that further weakens the ability to self-monitor and further undermines goal pursuit, or any further attempt at self-regulation (i.e., no monitoring, no self-control).

It’s not a pretty picture, is it? But it’s certainly one that I think every human being knows. It’s that downward spiral we experience when “we don’t feel like it” and negative emotions begin to “weave their tendrils” (as these authors depict) throughout our self-regulatory process.

Interestingly, Wagner and Heatherton paint this despairing picture even a little darker, writing:

“Throw in the fact that prior self-regulatory effort may leave the individual in a depleted state in which both resources for further self-control are lacking and the strength of impulses and temptations are increased, and it is a small miracle that people are not constantly acting out their fantasies, drinking, smoking, or indulging in every gastronomic desire.”

This is indeed a pretty dire picture, and it’s not helped by the fact that there is very little research documenting how positive emotions might reverse this. Although there is some evidence to suggest that positive emotions might buffer against ego-depletion and enhance self-regulation, positive emotions are not simply the antidote. In fact, positive emotions might feed further off-task behaviors if this becomes the new focus of attention; a sort of carpe diem or even “what the hell” effect where we give in and decide it’s time to eat, drink and be merry.

The authors end with this sentence:

“Negative affect is thus a particularly potent threat to self-regulation, because it not only reduces the capacity for control (increased working memory load, reduced self-awareness and monitoring) but it may also lead to increases in the strength of experienced desires and emotions, rendering them all the more difficult to resist.”

So, you might ask as you join me in this dark place, “what are we to do?” How do we manage to self-regulate? Well, this has been the focus of most of my blog writing over the past years, with all sorts of strategies derived from a variety of different studies.

In my last blog post, I re-emphasized the importance of not paying attention to these emotions when they arise. Not a simple thing, I understand, as I noted above that negative emotions (affect) are related to and even seem to cause rumination. This rumination is the antithesis of “not paying attention.” But you get my point, right? The research summarized in this chapter makes it clear that negative emotions really do undermine self-regulation through processes like rumination that puts too much load on working memory (which derails monitoring our goal pursuit), or by provoking a hedonic response to feel good now.

Gross offers some potential points of intervention in his own process model of emotion. And, although it’s simply not possible to go much further in a single blog post, I will note that one effective strategy that is incorporated into many successful procrastination interventions is learning to modify appraisals of our situation to alter its emotional significance (I’ll come back to this at some other time, as this was part of the work we did in our recent book Procrastination, Health and Well-Being). In any case, the focus here is on cognitive change, the kind emphasized in cognitive behavioral therapies, for example.

I hope that you can see that despite the “poison tendrils” of negative emotions depicted so vividly by Wagner and Heatherton, there are routes to self-regulatory success. For some of us, this is certainly made more difficult by personality traits such as low emotional stability, as we are more chronically attuned to negative emotions. However, we can learn to act out of character as we learn new strategies to cope. Strategies that are much more effective than avoidance, self-blame and behavioral disengagement, each of which has been demonstrated to be risks not only to our success, but to our health.

This guest article originally appeared on PsychCentral.com: The Poison Tendrils of Negative Emotions by Timothy A Pychyl Ph.D.

References

Pychyl, T.A., & Sirois, F.M. (2016). Procrastination, emotion-regulation and well-being. In F.M. Sirois & T.A. Pychyl, (Eds.), Procrastination, health and well-being (pp. 163-188). New York: Elsevier.

Sirois, F.M. (2015). Is procrastination a vulnerability factor for hypertension and cardiovascular disease? Testing an extension of the procrastination-health model. Journal of Behavioral Medicine, 38, 578-589. DOI: 10.1007/s10865-015-9629-2

Wagner, D.D. & Heatherton, T.F. (2014). Emotion and self-regulation failure. In J. J. Gross (Ed.), Handbook of emotion regulation (pp. 613-628). New York: The Guilford Press.

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Sweden to investigate sex lives

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NHS England boosts GP retained doctor scheme

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Ocean-cleaning sea bins will gobble up plastic waste to recycle

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NHS England acts on rising GP indemnity costs

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NHS England offers GP practices millions in practice development support

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£40m fund to support struggling practices available

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Autoimmune diseases may be side effect of a strong immune system

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Multispecialty community provider contract options unveiled

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'We want women to feel safe'

The UK's first maternity service for victims of rape and sexual abuse, which opens today at the Royal London Hospital. via BBC News - Health Read More Here..

On The Pulse - July 2016

Exercise is as effective as arthroscopic menisectomy for patients with knee pain

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Inbreeding has destroyed the English bulldog’s genetic diversity

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Fossil tumour is oldest evidence of human cancer discovered yet

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Complaining and the Brain – How “Bad Karma” Is Created

It is intuitive that a negative attitude and constant complaining are bad for us – but can it really affect our brain? It turns out that there is a growing body of evidence suggesting that negativity can alter our perception of life by changing the connection of the neurons in our brain. This would then result in increased stress levels, which is linked to chronic diseases and mental health problems.

A common perception of complaining, or “venting”, is that people feel better after getting their emotions out. Contrary to popular belief, however, studies have shown that expressing negativity can be bad for the mood of both the complainer and the listener, and here we briefly discuss a few findings on how negativity can impact our well-being.

Do negative thoughts affect the wiring of synapses in our brains?

The synapses in our brain are separated by spaces known as synaptic clefts. When we think, synapses “fire” and send signals across these clefts to other synapses. This forms a bridge by which signals and information and transferred. The exciting thing here is that upon each trigger of an electrical charge, the synapses involved are actually brought closer in proximity to each other. This increases the likelihood that the correct synapses will share the appropriate link and fire together. Consequently, it becomes easier for that particular thought to be triggered.

What all this means is that thinking about something initially makes it easier to think about it again in the future. As such, if a person is constantly unhappy, it makes it more likely that he or she will continue to have negative thoughts if nothing is done about it. On the bright side, though, this also suggests that if we make a conscious effort to think positive thoughts, the positive feedback cycle helps us to become a more optimistic personality as well.

By repeating pessimistic thought processes, synapses that represent these negative inclinations gradually grow closer. Given that the thought that is most likely to surface is the one which can form a bridge between synapses in the shortest period of time, it is unsurprising then that in this case a pessimist would be more likely to remain the way he or she was.

Who we spend time with can change our thinking subconsciously

In view of how negativity can change our behaviour, it is perhaps not all that surprising that who we spend our time with influences our brain as well. The basis of this is primarily linked to how we empathize with others. For instance, when we see another person experiencing some emotion such as joy, sorrow or anger, our brain attempts to fire the same synapses to relate to the observed emotion.

By trying to imagine what the other person is going through, this rewiring of our brain (or the phenomena of “mirror neurons”) can in fact contribute to our patterns of thought without us realizing it – in fact, the activation of this mirror neuron system has been shown in a study to be altered in adolescents with autism spectrum disorder (ASD). These findings were reported based on functional magnetic resonance imaging (fMRI) data on how brain activation differs between the ASD group and the control group when inferring the intention of an action. Therefore, it would then be logical that if we surround ourselves with people who are generally optimistic, our inclinations towards happy interactions would be greatly enhanced.

Stress can affect our health more directly than we think

In addition to hurting our mental well-being, the act of venting can be detrimental to our physical health as well. For example, anger-related synaptic firing can be bad for our immune system when coupled with an increase in blood pressure, as well as a higher risk of conditions such as obesity, diabetes and heart problems.

The main contributing factor to all the negative effects of stress is a hormone in our body known as cortisol. This has been dubbed a “stress hormone”, as the levels of this hormone in our body are drastically elevated when we feel stressed out. In this regard, the release of cortisol by our adrenal glands in response to stressors such as fear is an integral component of our fight-or-flight mechanism. However, prolonged release leads to impaired learning and memory, higher cholesterol levels and blood pressure, and a weakened immune system.

To date, there are numerous studies which demonstrate the profound negative effects of stress on our physical and mental health. For example, it has been shown that cortisol production induced by social aggression and isolation can be a powerful trigger for mental disorders and reduced resilience, particularly for adolescents. To this end, scientists subjected mice that were genetically predisposed to mental illness to social isolation during adolescence. This triggered marked behavioural abnormalities that persisted even when the mice were returned to the group. More importantly, the effects of isolation stretched all the way into adulthood, implying that adolescent stress can cause long-term damage to mental health.

In another study, scientists specifically bred mice to be “bullies”, and then subjected other mice to aggression from these bullies. They found that the “bullied” mice would release cortisol that subsequently led to increased social aversion to other mice. Moreover, this “scared” behaviour in bullied mice disappeared when the cortisol receptors were blocked, indicating that excessive cortisol could lead to decreased resilience.

Taken together, the aforementioned findings highlight the negative effects of stress and could be implicated in the development of treatments for depression and other devastating psychiatric disorders. Additionally, they also suggest that in adolescents predisposed to mental illnesses, efforts to protect them from social stressors such as bullying and neglect could go a long way in reducing the risk of getting these diseases.

References

Barik, J., Marti, F., Morel, C., Fernandez, S., Lanteri, C., Godeheu, G., Tassin, J., Mombereau, C., Faure, P., & Tronche, F. (2013). Chronic Stress Triggers Social Aversion via Glucocorticoid Receptor in Dopaminoceptive Neurons Science, 339 (6117), 332-335 DOI: 10.1126/science.1226767

Libero, L., Maximo, J., Deshpande, H., Klinger, L., Klinger, M., & Kana, R. (2014). The role of mirroring and mentalizing networks in mediating action intentions in autism Molecular Autism, 5 (1) DOI: 10.1186/2040-2392-5-50

Markram, H. (2011). A history of spike-timing-dependent plasticity Frontiers in Synaptic Neuroscience, 3 DOI: 10.3389/fnsyn.2011.00004

Niwa, M., Jaaro-Peled, H., Tankou, S., Seshadri, S., Hikida, T., Matsumoto, Y., Cascella, N., Kano, S., Ozaki, N., Nabeshima, T., & Sawa, A. (2013). Adolescent Stress-Induced Epigenetic Control of Dopaminergic Neurons via Glucocorticoids Science, 339 (6117), 335-339 DOI: 10.1126/science.1226931

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Cheat's guide

Scientists say that having just an hour of exercise a day may help undo the damage of sitting at a desk all day. Here are five tips on how to be more active without having to go anywhere near a gym. via BBC News - Health Read More Here..

Cancer found in ancient human ancestor's foot

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Exercises you can do at your desk to counter sedentary job

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Hour of Exercise a Day May Offset Sitting's Toll on Health

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Exercise May Keep Diabetes in Check During Pregnancy

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Lack of Fitness Second Only to Smoking as Predictor of Early Death

Increases in fitness levels were associated with greater longevity

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CRISPR genome editing could save sight by tweaking DNA

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EEG scans could help determine awareness in vegetative states

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One hour of exercise can undo the damage from sitting all day

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Weight loss surgery linked with increased fracture risk

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Human nose study yields new antibiotics

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Hour's activity 'offsets sedentary day'

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Desk job death risk is eliminated by an hour’s walk or cycle

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Florida investigates four mysterious Zika infections

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Ice Bucket Challenge mum praises ALS 'breakthrough'

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Legal ketone sports supplement pushes athletes further, faster

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Ice Bucket Challenge funds gene discovery in ALS (MND) research

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Drug 'may slow' Alzheimer's brain death

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Unprecedented Alzheimer’s drug slows disease by 80 per cent

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Supervised self-monitoring improves diabetes control

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Bedroom battleground

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WHO and Ministry of Health expand cholera response to minimize future risk

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Cannabinoids Hold Promise for Alzheimer’s Disease Treatment

Alzheimer’s disease (AD) is a neurodegenerative condition and the most common form of dementia worldwide, accounting for around 70% of dementia cases. Deposition of the amyloid-beta (A-beta) peptide in the form of amyloid plaques is one of the hallmarks of the disease, occurring early in the development of this condition. As disease progresses, degenerative changes accumulate, leading to neuronal death, oxidative damage, and neuroinflammation.

The exact pathological mechanisms that drive Alzheimer’s disease remain to be clarified and are the subject of extensive research (and debate). With the goal of further elucidating some of the processes that drive Alzheimer’s progression, new research published in the Nature Partner Journal Aging and Mechanisms of Disease studied the association between A-beta accumulation and the development of neuroinflammation, as well as possible therapeutic interventions. Their results were promising.

Does A-beta accumulation cause inflammation?

Neuroinflammation is a characteristic of the aging process and is one of the main causes of cognitive impairment. In the context of neurodegenerative diseases, inflammatory responses are further increased and contribute to the accelerated rate of cognitive decline that is observed. The increased inflammatory response found in the brain of Alzheimer’s patients has been mostly regarded as a consequence of the activation of glial cells in the brain.

This study, carried out in vitro, indicates that this may not be so: it establishes a direct link between A-beta and inflammation, demonstrating that A-beta production in cultured human central nervous system neurons leads to the synthesis of a number of proinflammatory molecules and to the activation of inflammatory pathways. Most of the proinflammatory molecules known to be excessively produced in the brain of Alzheimer’s patients were shown to also be overproduced in neurons after the induction of A-beta production.

Furthermore, these results suggest that A-beta production in neurons may induce inflammation even before it starts accumulating and forming amyloid plaques in the brain.

Are NSAIDs a bad choice for Alzheimer’s patients?

Non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to delay clinical features of Alzheimer’s disease, but clinical trials have never supported that idea. NSAIDs act by inhibiting a family of enzymes called cyclooxygenases (COX), which are responsible for the production of prostaglandins. Since prostaglandins can induce inflammatory responses, the inhibition of COX by NSAIDs results in decreased inflammation. Since COX-2 is known to be increased in the brain of Alzheimer’s patients, in theory, blocking the action of COX-2 using NSAIDs should be beneficial.

But the regulation of inflammation is not the only function of prostaglandins, which actually depends on the receptors they activate. As it turns out, according to this study, the prostaglandins PGE2 and PGD2 are actually neuroprotective, similarly to what has been found in ischemic stroke and in other neurodegeneration models. The increase in COX-2 production may therefore be a defense mechanism that neurons set in motion. By inhibiting this defense system, NSAIDs may actually promote further cellular damage.

This work showed that the detrimental action of A-beta can be mediated by the action of molecules produced by another enzyme called 5-lipoxygenase (5-LOX). These molecules, called leukotrienes, seem to be the ones that potentiate A-beta’s toxicity. It was shown that the inhibition of 5-LOX was able to prevent cell death, therefore holding better therapeutic potential than NSAIDs.

Cannabinoids effectively block A-beta toxicity

Interestingly, both prostaglandins and leukotrienes derive from the same molecule: arachidonic acid. And arachidonic acid is also a component of a family of endogenous cannabinoids produced in the brain.

Cannabinoids had already been studied in the context of Alzheimer’s disease, having been shown that they can reduce A-beta accumulation and improve memory. Not only endogenous cannabinoids, but also tetrahydrocannabinol (THC), the main psychoactive component of cannabis, are also known to be able to reduce inflammation.

Therefore, this study also investigated whether cannabinoids could have therapeutic potential for Alzheimer’s disease. It was shown that an endocannabinoid called arachidonoyl ethanol amide (AEA), as well as synthetic analogs to this molecule, could promote neuronal survival and block A-beta accumulation. The inhibition of the enzyme that degrades AEA was also shown to be protective.

THC was also tested in this study and the results were very promising: THC had a marked protective effect, being able to remove intraneuronal A-beta, to dramatically reduce the elevated production of damaging leukotrienes, and to block neuronal cell death.

The results of this study show that cannabinoids may indeed hold promise for the treatment of Alzheimer’s disease. It remains to be determined if similar effects will also be obtained in vivo.

References

Bayer, . (2010). Intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease Frontiers in Aging Neuroscience DOI: 10.3389/fnagi.2010.00008

Burstein, S., & Zurier, R. (2009). Cannabinoids, Endocannabinoids, and Related Analogs in Inflammation The AAPS Journal, 11 (1), 109-119 DOI: 10.1208/s12248-009-9084-5

Campbell, V., & Gowran, A. (2009). Alzheimer’s disease; taking the edge off with cannabinoids? British Journal of Pharmacology, 152 (5), 655-662 DOI: 10.1038/sj.bjp.0707446

Currais, A., Quehenberger, O., M Armando, A., Daugherty, D., Maher, P., & Schubert, D. (2016). Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids npj Aging and Mechanisms of Disease, 2 DOI: 10.1038/npjamd.2016.12

Kim, E., Kwon, K., Park, J., Lee, S., Moon, C., & Baik, E. (2002). Neuroprotective effects of prostaglandin E2 or cAMP against microglial and neuronal free radical mediated toxicity associated with inflammation Journal of Neuroscience Research, 70 (1), 97-107 DOI: 10.1002/jnr.10373

Martín-Moreno, A., Brera, B., Spuch, C., Carro, E., García-García, L., Delgado, M., Pozo, M., Innamorato, N., Cuadrado, A., & de Ceballos, M. (2012). Prolonged oral cannabinoid administration prevents neuroinflammation, lowers ?-amyloid levels and improves cognitive performance in Tg APP 2576 mice Journal of Neuroinflammation, 9 (1) DOI: 10.1186/1742-2094-9-8

Valera, E., Dargusch, R., Maher, P., & Schubert, D. (2013). Modulation of 5-Lipoxygenase in Proteotoxicity and Alzheimer’s Disease Journal of Neuroscience, 33 (25), 10512-10525 DOI: 10.1523/JNEUROSCI.5183-12.2013

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Nurturing The Brain – Part 10, Ketogenic Diets

Fasting has been used as a form of therapy for epilepsy throughout the history of medicine. But in 1921, Dr Woodyatt at Rush Medical College in Chicago observed that that there were a couple of ketone molecules that appeared in the blood of subjects undergoing starvation or low-carbohydrate/high-fat content diets, while Dr Wilder at the Mayo Clinic proposed that similar effects to those of fasting on epilepsy could be obtained by inducing the production of those same molecules through diet.

This was the origin of ketogenic diets, which became one of the most widely used treatments for epilepsy in children. It is still used to this day as an alternative to pharmacological treatments, although it is not known how it works.

The ketogenic diet is characterized by a continued intake of low amounts of carbohydrates, high doses of fat, and regular amounts of protein. This changes our body’s metabolism by turning fat into our main fuel: Instead of obtaining energy primarily from carbohydrates, our body obtains energy from stored fat and becomes more efficient at using fat as the main energy source. Although the intake of fat is higher, the net result is loss of stored fat.

Ketogenic low-carbohydrate/high-fat diets have been shown to be highly effective in promoting weight loss. They are called ketogenic because they lead to the production of molecules known as ketone bodies.

Ketone bodies, our brain’s other fuel

Glucose is our body’s primary source of energy. When regular amounts of carbohydrates are ingested, our carbohydrate stores keep being replenished and glucose keeps being used as fuel. But when blood glucose levels drop and carbohydrate stores are exhausted, fats stored in adipose tissue are broken down and free fatty acids are released into the blood.

Fatty acids are then taken up by cells to be used to produce energy. This happens, for example, during periods of carbohydrate restriction, fasting or starvation, or prolonged intense exercise.

However, fatty acids cannot cross the blood-brain barrier and therefore cannot be used by neurons and glia in the central nervous system. However, the liver can use acetyl-CoA obtained from fatty acid metabolism to produce ketone bodies – acetone, beta-hydroxybutyrate and acetoacetate. Ketone bodies are able to cross the blood-brain barrier and can be used as a replacement for glucose in the brain.

One of the reasons why ketogenic diets are often more effective than low-fat diets in promoting weight loss is the fact that ketone bodies may actually suppress appetite by acting on the hypothalamus, where signals from appetite-regulating hormones such as leptin or ghrelin are combined, by interacting with these hormonal signals.

Ketone bodies and brain health

The effects of ketogenic diets are not limited to seizure prevention. Ketogenic diets have shown beneficial effects and are being studied as therapeutic options for an impressively high range of neurological disorders: cognitive impairment, migraine, pain, traumatic brain injury, stroke, Alzheimer’s disease, Parkinson’s disease, sleep disorders, autism, amyotrophic lateral sclerosis and multiple sclerosis, for example.

This effect may be due to a neuroprotective action of ketone bodies. Although the mechanisms are poorly understood, studies in animal and cellular models have shown that ketone bodies can protect neuronal and glial cells against different types of cellular injury and even death. It is believed that this effect may be due to increased energy production and energy storage, since ketone bodies are actually more effective energy sources for neurons. This may arm neurons with an improved ability to resist metabolic insults.

Importantly, ketone bodies can have antioxidant and anti-inflammatory effects. Oxidation and inflammation are the main motors of aging and of a number of pathologies, particularly neurodegenerative diseases. By reducing oxidative stress and chronic inflammation, ketogenic diets can delay aging and delay or even decrease the development of many of the diseases mentioned above.

Furthermore, ketogenic diets are effective routes to weight loss, as already mentioned; since obesity has been associated with – for example, accelerated cognitive decline and increased risk of dementia, Alzheimer’s disease and stroke – weight loss by itself can bring great benefits to brain health.

Another important therapeutic action of ketogenic diets may be an anti-cancer effect. Cancer cells have high metabolic rates that allow their fast proliferation. It is possible that depriving these cells from glucose, the fuel they grew on, may hamper their growth. Research has shown that animals with brain tumors that are placed on a ketogenic diet show a marked decrease in the rate of tumor growth, most likely due to the lack of glucose. There are even case reports of humans with brain tumors who have greatly improved due to the adoption of a ketogenic diet.

But besides the neurological effects of ketogenic diets, there are many other health benefits described for a ketone-based metabolism. Ketogenic diets can decrease both plasma glucose and insulin concentrations, decreasing the likelihood of developing type 2 diabetes and other metabolic diseases; the levels of blood triglycerides can also be diminished, LDL cholesterol can be reduced and HDL cholesterol can be increased, thereby also decreasing the risk of cardiovascular diseases.

It is arguable that evolution hasn’t prepared us for the amount of carbs we ingest. Maybe we would be better off running on ketone bodies.

References

Barañano, K. W., & Hartman, A. L. (2008). The ketogenic diet: Uses in epilepsy and other neurologic illnesses. Current Treatment Options in Neurology, 10(6), 410–419. doi:10.1007/s11940-008-0043-8

Gano, L. B., Patel, M., & Rho, J. M. (2014). Ketogenic diets, mitochondria, and neurological diseases. The Journal of Lipid Research, 55(11), 2211–2228. doi:10.1194/jlr.r048975
Gasior, M., Rogawski, M. A., & Hartman, A. L. (2006). Neuroprotective and disease-modifying effects of the ketogenic diet. Behavioural Pharmacology, 17(5-6), 431–439. doi:10.1097/00008877-200609000-00009

Gibson, A. A., Seimon, R. V., Lee, C. M. Y., Ayre, J., Franklin, J., Markovic, T. P., … Sainsbury, A. (2014). Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Obesity Reviews, 16(1), 64–76. doi:10.1111/obr.12230

Kinzig, K. P., Honors, M. A., & Hargrave, S. L. (2010). Insulin sensitivity and glucose tolerance are altered by maintenance on a Ketogenic diet. Endocrinology, 151(7), 3105–3114. doi:10.1210/en.2010-0175

Klein, P., Tyrlikova, I., & Mathews, G. C. (2014). Dietary treatment in adults with refractory epilepsy: A review. Neurology, 83(21), 1978–1985. doi:10.1212/wnl.0000000000001004

Seyfried, T. N., Marsh, J., Shelton, L. M., Huysentruyt, L. C., & Mukherjee, P. (2012). Is the restricted ketogenic diet a viable alternative to the standard of care for managing malignant brain cancer? Epilepsy Research, 100(3), 310–326. doi:10.1016/j.eplepsyres.2011.06.017

Stafstrom, C. E., & Rho, J. M. (2012). The Ketogenic diet as a treatment paradigm for diverse neurological disorders. Frontiers in Pharmacology, 3. doi:10.3389/fphar.2012.00059

Wheless, J. W. (2008). History of the ketogenic diet. Epilepsia, 49, 3–5. doi:10.1111/j.1528-1167.2008.01821.x

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