“What is known of the moral effects of different foods? Is there any philosophy of nutrition?”
—Friedrich Nietzsche, The Gay Science
James T. Hong, in his 2017 lecture “On Nietzsche’s Second Brain”, embodies the vital philosopher-scientist perspective, conflating Nietzsche’s philosophical ideas to his dietary experiments and subsequent changes that may have been occurring in his microbiome.
“All prejudices may be traced back to the intestines.”
—F. Nietzsche, Ecce Homo
The gut microbiome is constantly communicating with the brain, affecting our mood, cognition, and, as a downstream trajectory, our decisions and personality (Johnson, 2020).
“The reason why these individuals have different feelings and tastes is usually to be found in some oddity of their lifestyle, nutrition, or digestion…”
—F. Nietzsche, The Gay Science
Hong comes across as personable, frenetic, and curious. His understanding of nutrition and microbiota is admittedly cursory, but he’s already ahead of the curve of mainstream medical culture by knowing about the gut-brain axis: psychobiotics, intestinal permeability, fecal transplants and their relationship to mental health and the immune system.
Hong contemplates whether Nietzsche’s insanity resulted from decades of extreme dietary experimentation ruining his gut microbiome. The reasoning is as follows: when we restrict food groups, the bacteria that produce enzymes to help us digest that food go dormant or extinct, so someone like Nietzsche who underwent dietary extremes resembling fruitarianism and carnivorism, deranged his microbiome so drastically that it eventually couldn’t accommodate his digestion or cognition. I have yet to find evidence to support this reasoning as it applies to the human organism, and to the contrary, it is seen that dietary changes “rapidly and reproducibly” change the human gut microbiome, meaning that any changes resulting from addition or restriction of foods are reversible (David, et al., 2014).
The toxic effects of agricultural and industrial foods that humans are not evolutionarily adapted to consume are for more likely the reason for progressively ruined microbiota: that is, grains, dairy, and industrial additives.
Nietzsche was driven to dietary experimentation by the severity of his preexisting symptoms, such as migraine, visual problems, indigestion, insomnia, and depression. These were mostly transient, with periods of relief and profound reinvigoration followed by painful relapses, sometimes requiring days of bedrest. His health struggles, combined with his growing frustration toward Schopenhauer’s pessimistic life-negation, led him to advocate an affirmation and reverence toward one’s own suffering, and the collective suffering in all existence.
“The discipline of suffering, of great suffering—know ye not that it is only this discipline that has produced all the elevations of humanity hitherto?”
—F. Nietzsche, Beyond Good and Evil
Valeria Silvestri proposes Nietzsche’s bad health is explained by Takayasu’s arteritis, an autoimmune disease that damages blood vessel walls. Nietzsche’s father died at 36 of stroke, his younger brother had migraines, and Nietzsche’s downfall was preceded by at least three strokes. Speculation on Nietzsche’s illness continues indefinitely, but the hypotheses all revolve around vascular, mitochondrial, and neuronal inflammation (Tényi, 2012).
Eva Cybulska thinks Nietzsche exhibited signs of bipolar disorder (2016). His intimacy with intense, alternating moods, and his grandiose philosophical prose, presumably written during periods of “mania”, would support this. Cybulska points out that his fall into insanity and catatonia from age 39 until his death was possibly a severe presentation of dementia. Those with bipolar disorder have a three-fold increased risk of developing dementia (Velosa, et al., 2020).
Dementia is as much mitochondrial as it is neurological, and the chronic health problems Nietzsche fought against were an unfortunate warning of mitochondrial dysfunction. The mitochondria of bipolar patients are smaller and congregate to abnormal regions of the cell (Cataldo, et al., 2010) and a novel area of neuropsychopharmacology involves treating bipolar and other psychiatric illness with mitochondrial enhancers (Pereira, et al., 2018).
Much of mental illness, including bipolar disorder, is related to inflammation or toxicity of the gut-brain axis. For example, bipolar 1 patients and schizophrenics have significantly elevated immunoglobulin-G antibodies to gliadin in wheat and casein protein in dairy (Severance, et al., 2010; Neibuhr, et al., 2011; Dickerson, et al., 2012).
Nietzsche’s morning routine included a 7 a.m. glass of warm milk before beginning to write, “when not felled by headaches and vomiting”. He ate meat and “unbelievable” amounts of fruit for lunch, to the point of indigestion, and gorged on bread and honey before bed. At times, he lived purely on sour-milk. If he had food sensitivities, which his symptoms combined with novel research would suggest, he was unknowingly being poisoned morning and night for years.
In dementia, which is increasingly referred to as “diabetes type 3”, the neurons become insulin resistant, or incapable of utilizing glucose for energy. The A1 beta-casein protein in dairy produces diabetic insulin resistance in mice that worsens with each subsequent generation of offspring consuming dairy (Chia, et al., 2018). Infants who are fed cow’s milk instead of being breastfed have persistently higher intestinal permeability (Weaver, 1988), setting the stage for brain inflammation, and a randomized controlled trial found that those drinking A1 beta-casein milk had long-term lower cognitive abilities and higher overall inflammation and indigestion (Jianqin, et al., 2016). Intestinal permeability precedes the onset of type 1 diabetes (Bosi, et al., 2006), and milk’s A1 beta-casein enhances permeability and produces either autoimmune diabetes or insulin resistance in significant subsets of mice (Chia, et al., 2017).
Chronic digestive disorders are predictive of the development of depression and vice versa (Blackwell, et al., 2020). Those with inflammatory bowel disease are diagnosed with dementia at much earlier ages, and their dementia risk increases with the severity of bowel symptoms (Zhang, et al., 2020).
The short chain fatty acids such as butyrate, produced by beneficial bacteria in the gut, translocate to the brain and offer protective and restorative effects. In the absence of these beneficial strains, and with the presence of pathogenic bacteria and its byproduct endotoxin translocating their components into the bloodstream and brain, systemic symptoms and neurodegeneration are the natural consequences (Marizzoni, et al., 2020).
Transplanting the intestinal bacteria from healthy wild-type mice into mice bred to develop Alzheimer’s reduced brain amyloid plaque and tau protein accumulation, and improved cognitive impairment, in the Alzheimer’s-mice. Epigenetic changes occured in the colons of the Alzheimer’s mice, related to a calming of their chronic inflammation. The Alzheimer’s-mice had leaky intestinal barriers and chronically inflamed colons to begin with, and the treatment that restored their brain homeostasis didn’t involve focusing on their brains at all (Kim, et al., 2018).
Other factors in neuropsychiatric illness, such as stress, trauma, and genetics, are in interplay with the intestines. Stress increases intestinal permeability (the tight junctions become inappropriately loose), leaking endotoxin and allergens into the abdominal cavity and bloodstream, paving the way for a leaky blood-brain barrier and neurodegeneration.
Trauma has long-lasting effects on the microbiome, and alters genes through methylation and acetylation that increase the likelihood of intestinal issues and subsequent mental issues later in life (Callaghan, et al., 2019). Nietzsche lost his father at a young age, experienced lifelong alienation, was rejected and heartbroken by his only major romantic interest, and generally brooded over his opposition to contemporary society as a whole. The mental weight of his philosophy and experiences took their toll.
For I wish this to be understood; it was during the years of my lowest vitality that I ceased from being a pessimist: the instinct of self-recovery forbade me a philosophy of poverty and discouragement.
—F. Nietzsche, Ecce Homo
Nietzsche staved off his decline to the best of his ability with the knowledge available to him: his frequent mountain hikes and emphasis on exploratory physical movement in nature, his avoidance of cold and harsh climates, his obsession with learning and championing of a heroic optimism in spite of neuroticism and loneliness, all buffered the physiological insults. However, that same loneliness, heartache, and lack of connection he so frequently journaled of surely compounded with his inflammatory conditions to accelerate his degeneration, and he, being so physiologically intuitive, probably understood the consequences of such stressors.
The refinement of character and soul that potentially emerges from trauma and suffering is a separate phenomenon to the physiological damage that occurs: that which does not kill us makes us stronger, while breaking us down.
“Only great pain is the ultimate liberator of the spirit…I doubt that such pain makes us ‘better’; but I know that it makes us more profound.”
—F. Nietzsche, The Gay Science, section 3
What it means for us: the applicability of physiological principles
We’re living in a paradigm shift back toward holism that was unfortunately obfuscated over the last century by a biomedical culture dominated by Cartesian reductionism: the hyperspecialization and compartmentalization of experts and an aggression against innovation and openness in science and health. Industry fraud and profit supersede the ability of institutional guidelines to have our best interests, so developing an autonomous, proactive orientation to nutritional physiology, as Nietzsche attempted, can make a great difference in your overall state and trajectory of aging and illness.
Besides sunlight and herbal tinctures, biohacking modalities were obviously not available to Nietzsche (he did like morphine), but thankfully the information and equipment are there for those who need it today.
Red light therapy is a powerful mitochondrial enhancer, currently being studied in clinical trials for treatment of Parkinson’s Disease and bipolar disorder, and limited evidence shows efficacy for dementia. It has been used to accelerate healing after traumatic brain injury. Dan Wich at selftestable.com has a useful guide for inexpensive red light devices. I have used the Philips R40 Infrared Heat Lamp suspended in a Woods clamp reflector, since 2016, to good effect.
Simply removing the offending foods can be enough to put “incurable” diseases into remission. Heart disease, type 2 diabetes, epilepsy, mental illness, cancer, chronic fatigue, Parkinson’s, dementia, lupus, and multiple sclerosis have been improved or remitted by dietary intervention (Brunk, 2020; Gundry, 2018; Food Intolerance Network; MeatRx).
In susceptible people, high carbohydrate intake can increase excitability of the brain and nervous system to pathological levels, such as in epilepsy (Patel & Rho, 2012), schizophrenia, and bipolar disorder. The ketogenic diet, which limits carbohydrate intake to 20 grams maximum per day, causing the brain to substitute brain-calming ketone bodies for glucose, has been used clinically since the 1920s for treatment-resistant epilepsy, and is seeing a revival as it is used to relieve psychiatric and metabolic diseases (Norwitz, et al., 2020; Sarnay & Palmer, 2020).
For autoimmunity and inflammation, the most common offending agents are glutinous grains and dairy, followed by oxalates and lectins in certain plant foods (which sabotage mitochondria), rancid polyunsaturated fats in industrial vegetable oils, and salicylates and amines, common in aged foods. For insulinergic or metabolic disease, an experimental reduction or removal of carbohydrates, or fasting, is the solution for many. Others find ultimate relief with mercury detox via the Cutler Protocol (some think Nietzsche had mercury) or neural retraining therapies such as meditation, EMDR, DNRS, or the Gupta Program.
Under the right conditions, intermittent or extended fasting can heal brain pathology, for example, by reducing neuronal excitability or restoring deranged neurotransmitter metabolism. Fasting can be miraculous for the gut, encouraging homeostasis of the microbiome and restoration of proper intestinal barrier function, and for the brain, where neuronal autophagy occurs, clearing out damaged organelles and debris and spurring neurogenesis, the birth of new neurons. However, under the wrong conditions, it can exacerbate existing issues. Fasting increases cortisol when glucose metabolism shifts over to ketosis, and when the liver uses cortisol for gluconeogenesis, turning amino acids into glucose for energy. Too much cortisol induces insulin resistance, whereby glucose metabolism will be even less efficient upon refeeding.
Pair metabolic stress with exercise—Nietzsche would often walk eight hours per day—and overtraining syndrome can occur, characterized by heightened cortisol, insulin resistance, depression, and a leaky gut with concomitant systemic inflammation (Clark & Mach, 2016).
If one is “made of glass”, as Nietzsche proclaimed of himself, an extremely careful evaluation of every factor must be made at every turn.
A wound cannot heal if it is being continuously irritated. It is unfortunate those undue sufferings that occur when insufficient understanding by the culture makes the discovery of necessary information even less likely. Although the sufferings of the past act as building blocks that bestow insights onto future generations. In a year like 2020, previously unseen perspectives are needed more than ever before.
“Suddenly, many people are discovering that their conditions are oppressive, though they aren’t able to understand the causes […]
The existing educational systems aren’t going to help them to understand their place in the world, but that is the purpose of real education.”
—Ray Peat, “Education, a developmental process, confronts absolutism”, July 2020
“No can construct for you the bridge upon which precisely you must cross the stream of life, no one but you yourself alone.”
—F. Nietzsche, Untimely Meditations
Blackwell, Jonathan, et al. “Depression in Individuals Who Subsequently Develop Inflammatory Bowel Disease: a Population-Based Nested Case–Control Study.” Gut, 2020, doi:10.1136/gutjnl-2020-322308.
Callaghan, Bridget L., et al. “Mind and Gut: Associations between Mood and Gastrointestinal Distress in Children Exposed to Adversity.” Development and Psychopathology, vol. 32, no. 1, 2019, pp. 309–328., doi:10.1017/s0954579419000087.
Cataldo, Anne M., et al. “Abnormalities in Mitochondrial Structure in Cells from Patients with Bipolar Disorder.” The American Journal of Pathology, vol. 177, no. 2, 2010, pp. 575–585., doi:10.2353/ajpath.2010.081068.
Cate, Curtis. Friedrich Nietzsche. Overlook Press, 2005.
Chia, Joanne, et al. “Dietary Cows’ Milk Protein A1 Beta-Casein Increases the Incidence of T1D in NOD Mice.” Nutrients, vol. 10, no. 9, 2018, p. 1291., doi:10.3390/nu10091291.
Clark, Allison, and Núria Mach. “Exercise-Induced Stress Behavior, Gut-Microbiota-Brain Axis and Diet: a Systematic Review for Athletes.” Journal of the International Society of Sports Nutrition, vol. 13, no. 1, 2016, doi:10.1186/s12970-016-0155-6.
Cybulska, Eva M. Nietzsche and Bipolar Disorder, emcybulska.blogspot.com/2016/11/nietzsche-and-bipolar-disorder.html.
Cybulska, Eva M. “Nietzsche: Bipolar Disorder and Creativity.” Indo-Pacific Journal of Phenomenology, vol. 19, no. 1, 2019, pp. 51–63., doi:10.1080/20797222.2019.1641920.
David, Lawrence A., et al. “Diet Rapidly and Reproducibly Alters the Human Gut Microbiome.” Nature, vol. 505, no. 7484, 2013, pp. 559–563., doi:10.1038/nature12820.
Dickerson, Faith, et al. “Markers of Gluten Sensitivity in Acute Mania: A Longitudinal Study.” Psychiatry Research, vol. 196, no. 1, 2012, pp. 68–71., doi:10.1016/j.psychres.2011.11.007.
El-Mallakh, R.s., and M.e. Paskitti. “The Ketogenic Diet May Have Mood-Stabilizing Properties.” Medical Hypotheses, vol. 57, no. 6, 2001, pp. 724–726., doi:10.1054/mehy.2001.1446.
Hemmings, Sian M.j., et al. “The Microbiome in Posttraumatic Stress Disorder and Trauma-Exposed Controls.” Psychosomatic Medicine, vol. 79, no. 8, 2017, pp. 936–946., doi:10.1097/psy.0000000000000512.
Jianqin, Sun, et al. “Effects of Milk Containing Only A2 Beta Casein versus Milk Containing Both A1 and A2 Beta Casein Proteins on Gastrointestinal Physiology, Symptoms of Discomfort, and Cognitive Behavior of People with Self-Reported Intolerance to Traditional Cows’ Milk.” Nutrition Journal, vol. 15, no. 1, 2015, doi:10.1186/s12937-016-0147-z.
Johnson, Katerina V.-A. “Gut Microbiome Composition and Diversity Are Related to Human Personality Traits.” Human Microbiome Journal, vol. 15, 2020, p. 100069., doi:10.1016/j.humic.2019.100069.
Kato, Tadafumi, and Nobumasa Kato. “Mitochondrial Dysfunction in Bipolar Disorder.” Bipolar Disorders, vol. 2, no. 3, 2000, pp. 180–190., doi:10.1034/j.1399-5618.2000.020305.x.
Kim, Min-Soo, et al. “Transfer of a Healthy Microbiota Reduces Amyloid and Tau Pathology in an Alzheimer’s Disease Animal Model.” Gut, vol. 69, no. 2, 2019, pp. 283–294., doi:10.1136/gutjnl-2018-317431.
Marizzoni, Moira, et al. “Short-Chain Fatty Acids and Lipopolysaccharide as Mediators Between Gut Dysbiosis and Amyloid Pathology in Alzheimer’s Disease.” Journal of Alzheimer’s Disease, vol. 78, no. 2, 2020, pp. 683–697., doi:10.3233/jad-200306.
Muneer, Ather. “Bipolar Disorder: Role of Inflammation and the Development of Disease Biomarkers.” Psychiatry Investigation, vol. 13, no. 1, 2016, p. 18., doi:10.4306/pi.2016.13.1.18.
Niebuhr, David W., et al. “Association between Bovine Casein Antibody and New Onset Schizophrenia among US Military Personnel.” Schizophrenia Research, vol. 128, no. 1-3, 2011, pp. 51–55., doi:10.1016/j.schres.2011.02.005.
Norwitz, Nicholas G., et al. “Ketogenic Diet as a Metabolic Treatment for Mental Illness.” Current Opinion in Endocrinology, Diabetes & Obesity, vol. 27, no. 5, 2020, pp. 269–274., doi:10.1097/med.0000000000000564.
Patel, Manisha, and Jong M. Rho. “Sweets Are BAD for Seizures.” Epilepsy Currents, vol. 12, no. 6, 2012, pp. 218–219., doi:10.5698/1535-7511-12.6.218.
Pereira, Círia, et al. “Mitochondrial Agents for Bipolar Disorder.” International Journal of Neuropsychopharmacology, vol. 21, no. 6, 2018, pp. 550–569., doi:10.1093/ijnp/pyy018.
Phelps, James R., et al. “The Ketogenic Diet for Type II Bipolar Disorder.” Neurocase, vol. 19, no. 5, 2013, pp. 423–426., doi:10.1080/13554794.2012.690421.
Sarnyai, Zoltán, and Christopher M Palmer. “Ketogenic Therapy in Serious Mental Illness: Emerging Evidence.” International Journal of Neuropsychopharmacology, vol. 23, no. 7, 2020, pp. 434–439., doi:10.1093/ijnp/pyaa036.
Severance, Emily G, et al. “Immune Activation by Casein Dietary Antigens in Bipolar Disorder.” Bipolar Disorders, vol. 12, no. 8, 2010, pp. 834–842., doi:10.1111/j.1399-5618.2010.00879.x.
Silvestri, Valeria. “The ‘Eternal Recurrence’ of Arteritis. Suggesting Autoimmunity Underlining Friedrich Nietzsche’s Challenging Clinical Case.” Annals of Vascular Surgery, vol. 51, 2018, pp. 314–319., doi:10.1016/j.avsg.2018.03.020.
T;, Tényi. “The Madness of Dionysus — Six Hypotheses on the Illness of Nietzsche.” Psychiatria Hungarica : A Magyar Pszichiatriai Tarsasag Tudomanyos Folyoirata, U.S. National Library of Medicine, pubmed.ncbi.nlm.nih.gov/23429336/.
Velosa, J., et al. “Risk of Dementia in Bipolar Disorder and the Interplay of Lithium: a Systematic Review and Meta‐Analyses.” Acta Psychiatrica Scandinavica, vol. 141, no. 6, 2020, pp. 510–521., doi:10.1111/acps.13153.
Zhang, Bing, et al. “Inflammatory Bowel Disease Is Associated with Higher Dementia Risk: a Nationwide Longitudinal Study.” Gut, vol. 70, no. 1, 2020, pp. 85–91., doi:10.1136/gutjnl-2020-320789.