May 16, 2017
Written by Megan Roberts, MSc, and Tommy Wood MD, PhD
The ketogenic diet is becoming increasingly popular as we learn more about the potential benefits in terms of both performance and chronic disease management. However, the diet also has to be tailored to your personal goals, and we’ve previously written about some of the pitfalls for athletes using a ketogenic diet. For instance, satiety may be one of the most notable benefits of a ketogenic diet , which seems to provide an advantage during weight loss. But if you’re already lean and your ketogenic diet is causing you to undereat, losing lean mass can be a concern. This is important for athletes, but also for patients using a therapeutic ketogenic diet to control a chronic neurodegenerative disease, because muscle mass and strength are two of the best predictors of long-term health and mortality.
Thus, the question that naturally arises is: how can I implement a ketogenic diet without losing weight?
The topic of gaining or maintaining weight (specifically lean mass) on a ketogenic diet is often left out of the discussion. In fact, the following question was recently sent to the team at Nourish Balance Thrive:
I just finished listening to your latest podcast. Very informative!
At the end, you were asking for suggestions for possible topics. I have one: the combination of ketosis and an ectomorphic body type: issues for people like myself who don't want to lose weight or outright cannot afford to but want to apply ketosis for other reasons.
In my particular case, it is a neurodegenerative disease I'm dealing with (Parkinson's). There is quite a bit of literature indicating that a keto diet could be helpful, but my BMI varies between 19 and 20 and ketosis tends to lower that considerably.
Are there things one can tweak to do keto without the weight loss, or do you think it is simply a no-no? I think that the Parkinson’s aside, the question is relevant for more people.
Yes, we think so (given a well-formulated ketogenic diet with some specific modifications)!
While the root causes of brain cancer and neurological conditions such as Parkinson’s disease, Alzheimer's disease, and multiple sclerosis (MS) remain a hotly-debated topic, most experts agree that metabolic and mitochondrial dysfunction underlie many of the pathophysiologies.
Faulty insulin signaling may precede the neurocognitive and neuromuscular symptoms associated with Alzheimer’s disease, Parkinson’s disease, and MS [2, 3, 4]. Furthermore, increased insulin signaling likely promotes proliferation and survival of glioblastoma, a type of brain cancer . Abnormal glucose tolerance is also associated with these conditions [6, 7, 8]. Due to the fact that circulating ketone bodies provide an alternate fuel source for the brain , nutritional ketosis has been proposed as an adjunct therapy to combat the dysregulated energy metabolism that underpins many of the symptoms of neurodegenerative conditions, and may be a promising addition to the conventional chemotherapy treatment of brain tumors .
As mentioned above, many people experience increased satiety while eating a ketogenic diet. Some studies of the ketogenic diet also report a spontaneous reduction in calorie intake . While this can be great for those desiring to lose weight, it makes the diet potentially tricky to implement for someone who can’t afford to lose weight, or who is looking to gain muscle. Therefore, despite the fact that ketosis may be a promising therapy for individuals with neurodegenerative disease and cancer, the fact remains that these same individuals often struggle with weight loss and decreased appetite, especially as the conditions progress [11, 12, 13]. While there is both evidence and anecdote to suggest a muscle-sparing effect of ketones , which would be beneficial in patients with neurodegenerative disease, this is a highly-debated topic that we will save for a future post, and the evidence is far from conclusive.
This brings us to the main topic of this article:
Strength training is the most import stimulus for building and holding on to muscle regardless of your dietary choices. Resistance training may be especially important for improving strength, balance, and motor control in the context of a neuromuscular diseases such as Parkinson’s . Strength training may also improve symptoms and outcomes in individuals with cognitive impairment , MS , and cancer . When strength training, work up to at least three sessions a week and choose compound movements such as the squat, deadlift, bench press, overhead press, and row. If you’re not comfortable using weights, start with bodyweight movements like air squats, single leg Romanian deadlifts, push-ups, and pull-ups (or variations thereof). Blood flow restriction training  and super-slow resistance training, as described by Dr. Doug McGuff in his book Body by Science, are two safe and effective strategies to increase strength in injury-prone populations.
There is an abundance of evidence to suggest that aerobic exercise is beneficial for both neurodegenerative diseases [20, 21, 22] and cancer , not to mention just about every other chronic health condition known to man . But if you have trouble keeping weight on and preserving or gaining muscle mass, don’t go overboard on the endurance exercise. Instead, try lower-intensity activities such as walking. Everyone can benefit from more brisk walking, which has also been shown to increase quality of life in Parkinson’s patients . If you want to get the most bang for your buck, take a walk outside in the sun to get your daily dose of vitamin D, which likely plays an important role in neurological conditions . Better yet, listen to some music  on your walk.
Brain derived neurotrophic factor (BDNF) is a small protein that plays an important role in cognitive function. Since low levels of BDNF are implicated in neurodegenerative diseases [28, 29], finding ways to boost the level of BDNF in patients may be an important determinant of disease progression. And for the rest of us, increasing BDNF will help keep the brain sharp with age. Exercise, specifically intense exercise [30, 31], is not only one of the best ways to increase BDNF, but also has beneficial systemic effects that go above and beyond the brain. Furthermore, the ketone body beta-hydroxybutyrate may be an important player in the mechanism by which exercise increases BDNF expression .
It’s important to recognize that intensity will be determined on an individual basis. For instance, physical rehabilitation and seemingly moderate aerobic exercise has been shown to increase BDNF in Parkinson’s patients . This would be another ideal place to implement super-slow and/or blood flow restriction training to get the most bang-for-your-buck without risking injury. Given the context, there is no need to be doing hill sprints multiple times a week for extended periods of time, but occasionally partaking in an intense workout will allow you to reap the brain-boosting benefits of BDNF.
Despite the trend to disregard the “calories in, calories out” model of energy balance, calories do matter! If you want to implement a ketogenic diet without weight loss, you must pay attention to the quantity and quality of calories you’re consuming, since (as noted above) it can be easy to under-eat when in ketosis. It may even behoove you to track your meals for a few days using a tool like Senza to ensure you’re taking in enough calories.
While a ketogenic diet may not always be optimal for muscle building, it certainly can be done given enough dietary protein. Check out Ketogains for more on this. Keep in mind that you’re going to need to eat more protein than is sometimes recommended for a therapeutic ketogenic diet. A good place to start is 1.0-1.2 g/kg per day. Those using a therapeutic ketogenic diet for disease management could possibly bump protein intake up even higher on strength training days, so long as they’re able to stay in ketosis.
Like protein, dietary carbohydrates can be strategically manipulated to ensure you don’t lose too much mass on a ketogenic diet. Focus on consuming your carbs around exercise, which ideally should happen sooner rather than later in the day (especially if it’s intense). It’s worth playing with carb sources to find those that work for you without raising blood glucose, given that large swings in blood sugar should be avoided, especially in the context of therapeutic ketosis . Check out Robb Wolf’s 7-day carb test outlined in Wired to Eat to help you determine which carb sources work best for you, since blood glucose response to a given type of carbohydrate can be highly individual . You can even use a liberal amount of MCT oil in your higher-carb meals to keep ketones higher than they would be otherwise . Recognize that if you’re implementing a ketogenic diet in the context of brain cancer, it is more important to keep blood glucose (and therefore carbs) low in order to keep the glucose ketone index close to one .
There are multiple nutrients and corresponding nutrient deficiencies that have been associated with neurological conditions [37, 38, 39]. While the literature seems to be inconsistent regarding which supplemental nutrients actually work to help alleviate symptoms in a broader population, everyone can agree that eating a nutrient-dense, phytochemical-rich diet is important for overall health. This may be especially true for those with neurodegenerative conditions. For more on this, check out the brilliant work of Terry Wahls.
Ultimately, if seeking to maintain or gain weight, you should focus on eating both nutrient dense and calorie dense foods. Also, consume a variety of deeply pigmented fruits and vegetables to maximize the antioxidant and polyphenol content of your diet. You can use the Venn diagram below to help build a colorful plate that covers both nutrient and calorie density.
* Especially leafy greens, alliums (such as garlic and onions), crucifers, mushrooms
# Especially berries
^ Salmon, mackerel, anchovies, herring, sardines
≠ Grass fed and/or pasture raised
Given their nutrient profile, certain foods may be particularly efficacious for someone with a neurological condition. For example, liver is extraordinarily high in B vitamins . Cold-water fatty fish are the best sources of omega 3 fatty acids . Also, lion’s mane, a type medicinal mushroom, has been shown to be both neuroprotective and neuroregenerative .
Medium chain triglycerides (MCTs) are particularly ketogenic  and provide an easy way to increase the level of blood ketones. For the general population, we don’t recommend chasing a particular level of blood ketones, but for those with neurological conditions, higher ketones may be better . You can use MCT oil and/or powder liberally throughout the day to help you get into and stay in ketosis, even on your higher carbohydrate days .
MCTs have been shown improve cognitive function in individuals with Alzheimer’s disease . It stands to reason that other neurological conditions may also benefit from MCT supplementation, as caprylic acid (also known as octanoic acid or C8) can be both used by the brain itself or converted into ketones by astrocytes (a type of brain cell) [45, 46], although most of this conversion probably occurs in the liver. A note of caution with MCT products: add them into your diet slowly to minimize any unwanted GI distress.
While the utility of exogenous ketones is currently a topic of debate, perhaps their most promising application is in the realm of neurodegenerative disease (with athletic performance coming in as a close second). No studies to date have been done on humans, however d-β-Hydroxybutyrate has been shown to be neuroprotective in animal models of both Parkinson’s and Alzheimer’s disease .
We don’t advocate using exogenous ketones on top of a high-carb diet, as the metabolic implications of having high blood glucose and ketones simultaneously is unknown and likely unfavorable. The combination of glucose and supplemental ketones has been shown to raise insulin levels , which may be useful in specific situations (such as athletic performance) but is probably something to avoid for most individuals concerned with neurological health. However, for someone looking to reap the therapeutic benefits of ketosis while promoting muscle gain or halting unwanted weight loss, exogenous ketones may have a place.
We now know that fasting can be beneficial for many of the chronic diseases of aging . Fasting also has powerful effects on mitochondrial health, which is important to recognize given that mitochondrial dysfunction is associated with neurological conditions . Fasting protocols may even help alleviate symptoms in autoimmune conditions such as MS . However, fasting on a regular basis or even eating in a condensed time window can be a hindrance to someone who already has trouble maintaining weight.
Fortunately, fasting isn’t the only way to improve mitochondrial function. Exercise  and the ketogenic diet (in healthy controls) [53, 54] increase mitochondrial biogenesis, the making of new mitochondria. You can also support your mitochondria by eating a colorful, nutrient-dense diet. Recognize that fasting can be a great tool in the right situation - it should only be done if loss of body weight is not a concern or under the guidance of a physician. This might also be a smart place to use high-calorie Bulletproof coffee or tea - it turns out that constituents of coffee and tea may also be neuroprotective [55, 56].
This is perhaps the most important point of all: gut health is critical to success on a ketogenic diet. Even if you don’t present with overt gastrointestinal symptoms, poor gut health is strongly associated with neurological conditions and most of today’s chronic diseases. From an altered microbiome  to SIBO , H pylori , and fungal  infections, impaired gut health is clearly important to address for those with neurodegenerative conditions, and should probably be done before starting a ketogenic diet. If you try to add a ton of fat (especially saturated) on top of a leaky gut, you might even end up worsening your symptoms due to metabolic endotoxemia . Therefore, it’s important to fix any gut issues before dumping a load of fat into your system. Investing in a stool test under the guidance of a knowledgeable functional medicine practitioner is a smart first step, perhaps along with some digestive enzymes, probiotics, and/or fermented foods to support gut health.
Morning strength training and/or walk in the sunshine
Lunch: salad with loads of colorful veggies, sweet potato, sardines, nuts/seeds, avocado, olive oil, vinegar
Dinner: grass fed steak, a heap of veggies cooked in a healthy fat
Other: berries, coconut cream, dark chocolate, macadamia nuts, pemmican
It may take some intentionality, but if your portions are large enough and you don’t skimp on the fat, following this kind of nutrient-dense template can easily add up to a daily total of over 4,000 calories.
Remember context is key here. We’re trying to implement a therapeutic ketogenic diet to either gain lean mass or, at the very least, not lose weight. The average person looking to be in ketosis won’t have to be nearly as strategic with their nutrition and exercise choices. But for those with neurological conditions and/or those who want to gain or maintain weight on a ketogenic diet, some self-experimentation with the above recommendations might be in order.
If you need more help customizing your diet and training, book a free consultation. We’ll take a look at your personal history, identify possible root causes that are holding you back, and share how we’d approach your case as part of our “Elite Performance Program.”
1. Gibson, A. A., et al. "Do ketogenic diets really suppress appetite? A systematic review and meta‐analysis." Obesity reviews 16.1 (2015): 64-76.
2. Cunnane, Stephen C., et al. "Can ketones help rescue brain fuel supply in later life? Implications for cognitive health during aging and the treatment of Alzheimer’s disease." Frontiers in Molecular Neuroscience 9 (2016).
3. Moroo, I., et al. "Loss of insulin receptor immunoreactivity from the substantia nigra pars compacta neurons in Parkinson's disease." Acta neuropathologica 87.4 (1994): 343-348.
4. Oliveira, Sayonara Rangel, et al. "Disability in patients with multiple sclerosis: influence of insulin resistance, adiposity, and oxidative stress." Nutrition 30.3 (2014): 268-273.
5. Gong, Yuanying, et al. "Insulin-mediated signaling promotes proliferation and survival of glioblastoma through Akt activation." Neuro-oncology (2015): nov096.
6. Cunnane, Stephen C., et al. "Can ketones help rescue brain fuel supply in later life? Implications for cognitive health during aging and the treatment of Alzheimer’s disease." Frontiers in Molecular Neuroscience 9 (2016).
7. Lipman, Ivan J., Michael E. Boykin, and Roger E. Flora. "Glucose intolerance in Parkinson's disease." Journal of chronic diseases 27.11-12 (1974): 573-579.
8. Tieu, Minh Thi, et al. "Impact of glycemia on survival of glioblastoma patients treated with radiation and temozolomide." Journal of neuro-oncology 124.1 (2015): 119-126.
9. Hasselbalch, STEEN G., et al. "Blood-brain barrier permeability of glucose and ketone bodies during short-term starvation in humans." American Journal of Physiology-Endocrinology and Metabolism 268.6 (1995): E1161-E1166.
10. Branco, Ana F., et al. "Ketogenic diets: from cancer to mitochondrial diseases and beyond." European journal of clinical investigation 46.3 (2016): 285-298.
11. Abbott, R. A., et al. "Diet, body size and micronutrient status in Parkinson's disease." European journal of clinical nutrition 46.12 (1992): 879-884.
12. Gillette-Guyonnet, Sophie, et al. "Weight loss in Alzheimer disease." The American journal of clinical nutrition 71.2 (2000): 637s-642s.
13. Amitani, Marie, et al. "Control of food intake and muscle wasting in cachexia." The international journal of biochemistry & cell biology 45.10 (2013): 2179-2185.
14. Nair, K. Sreekumaran, et al. "Effect of beta-hydroxybutyrate on whole-body leucine kinetics and fractional mixed skeletal muscle protein synthesis in humans." Journal of Clinical Investigation 82.1 (1988): 198.
15. Chung, Chloe Lau Ha, Shamala Thilarajah, and Dawn Tan. "Effectiveness of resistance training on muscle strength and physical function in people with Parkinson’s disease: a systematic review and meta-analysis." Clinical rehabilitation 30.1 (2016): 11-23.
16. Mavros, Yorgi, et al. "Mediation of cognitive function improvements by strength gains after resistance training in older adults with mild cognitive impairment: outcomes of the study of mental and resistance training." Journal of the American Geriatrics Society 65.3 (2017): 550-559.
17. Kierkegaard, Marie, et al. "High-intensity resistance training in multiple sclerosis—An exploratory study of effects on immune markers in blood and cerebrospinal fluid, and on mood, fatigue, health-related quality of life, muscle strength, walking and cognition." Journal of the neurological sciences 362 (2016): 251-257.
18. Fairman, Ciaran M., et al. "A Scientific Rationale to Improve Resistance Training Prescription in Exercise Oncology." Sports Medicine (2017): 1-9.
19. Abe, Takashi, Charles F. Kearns, and Yoshiaki Sato. "Muscle size and strength are increased following walk training with restricted venous blood flow from the leg muscle, Kaatsu-walk training." Journal of Applied Physiology 100.5 (2006): 1460-1466.
20. Shu, Hai-Feng, et al. "Aerobic exercise for Parkinson's disease: a systematic review and meta-analysis of randomized controlled trials." PLoS One 9.7 (2014): e100503.
21. Dalgas, U., Egon Stenager, and Thorsten Ingemann-Hansen. "Review: multiple sclerosis and physical exercise: recommendations for the application of resistance-, endurance-and combined training." Multiple Sclerosis Journal 14.1 (2008): 35-53.
22. Morris, Jill K., et al. "Aerobic exercise for Alzheimer's disease: A randomized controlled pilot trial." PloS one 12.2 (2017): e0170547.
23. Cormie, Prue, et al. "The impact of exercise on cancer mortality, recurrence, and treatment-related adverse effects." Epidemiol Rev 39 (2017): 000-000.
24. Pedersen, Bente Klarlund, and Bengt Saltin. "Exercise as medicine–evidence for prescribing exercise as therapy in 26 different chronic diseases." Scandinavian journal of medicine & science in sports 25.S3 (2015): 1-72.
25. Uc, Ergun Y., et al. "Phase I/II randomized trial of aerobic exercise in Parkinson disease in a community setting." Neurology 83.5 (2014): 413-425.
26. Mpandzou, G., et al. "Vitamin D deficiency and its role in neurological conditions: A review." Revue neurologique 172.2 (2016): 109-122.
27. Raglio, Alfredo. "Music therapy interventions in Parkinson’s disease: the state-of-the-art." Frontiers in neurology 6 (2015).
28. Murer, M. G., Q. Yan, and R. Raisman-Vozari. "Brain-derived neurotrophic factor in the control human brain, and in Alzheimer’s disease and Parkinson’s disease." Progress in neurobiology 63.1 (2001): 71-124.
29. Wens, Inez, et al. "Brain derived neurotrophic factor in multiple sclerosis: effect of 24 weeks endurance and resistance training." European journal of neurology 23.6 (2016): 1028-1035.
30. Heyman, E., et al. "Intense exercise increases circulating endocannabinoid and BDNF levels in humans—possible implications for reward and depression." Psychoneuroendocrinology 37.6 (2012): 844-851.
31. Marston, Kieran J., et al. "Intense resistance exercise increases peripheral brain-derived neurotrophic factor." Journal of Science and Medicine in Sport (2017).
32. Sleiman, Sama F., et al. "Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate." Elife 5 (2016): e15092.
33. Frazzitta, Giuseppe, et al. "Intensive Rehabilitation Increases BDNF Serum Levels in Parkinsonian Patients A Randomized Study." Neurorehabilitation and neural repair 28.2 (2014): 163-168.
34. Meidenbauer, Joshua J., Purna Mukherjee, and Thomas N. Seyfried. "The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer." Nutrition & metabolism 12.1 (2015): 12.
35. Zeevi, David, et al. "Personalized nutrition by prediction of glycemic responses." Cell 163.5 (2015): 1079-1094.
36. Van Wymelbeke, Virginie, et al. "Influence of medium-chain and long-chain triacylglycerols on the control of food intake in men." The American journal of clinical nutrition 68.2 (1998): 226-234.
37. Seidl, Stacey E., et al. "The emerging role of nutrition in Parkinson's disease." Frontiers in aging neuroscience 6 (2014): 36.
38. da Silva, Sofia Lopes, et al. "Plasma nutrient status of patients with Alzheimer's disease: systematic review and meta-analysis." Alzheimer's & Dementia 10.4 (2014): 485-502.
39. Bitarafan, Sama, et al. "Dietary intake of nutrients and its correlation with fatigue in multiple sclerosis patients." Iranian journal of neurology 13.1 (2014): 28.
40. Sechi, GianPietro, et al. "Advances in clinical determinants and neurological manifestations of B vitamin deficiency in adults." Nutrition reviews (2016): nuv107.
41. Calviello, Gabriella, et al. "Experimental evidence of-3 polyunsaturated fatty acid modulation of inflammatory cytokines and bioactive lipid mediators: their potential role in inflammatory, neurodegenerative, and neoplastic diseases." BioMed research international 2013 (2013).
42. He, Xirui, et al. "Structures, biological activities, and industrial applications of the polysaccharides from Hericium erinaceus (Lion’s Mane) mushroom: A review." International Journal of Biological Macromolecules (2017).
43. Bach, Andrè C., and Virgen K. Babayan. "Medium-chain triglycerides: an update." The American Journal of Clinical Nutrition 36.5 (1982): 950-962.
44. Henderson, Samuel T., et al. "Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial." Nutrition & metabolism 6.1 (2009): 31.
45. Ebert, Douglas, Ronald G. Haller, and Marlei E. Walton. "Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy." Journal of Neuroscience 23.13 (2003): 5928-5935.
46. Auestad, Nancy, et al. "Fatty acid oxidation and ketogenesis by astrocytes in primary culture." Journal of neurochemistry 56.4 (1991): 1376-1386.
47. Kashiwaya, Yoshihiro, et al. "d-β-Hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease." Proceedings of the National Academy of Sciences 97.10 (2000): 5440-5444.
48. Holdsworth, David A., et al. "A Ketone Ester Drink Increases Postexercise Muscle Glycogen Synthesis in Humans." Medicine and science in sports and exercise (2017).
49. Wei, Min, et al. "Fasting-mimicking diet and markers/risk factors for aging, diabetes, cancer, and cardiovascular disease." Science translational medicine 9.377 (2017): eaai8700.
50. Gano, Lindsey B., Manisha Patel, and Jong M. Rho. "Ketogenic diets, mitochondria, and neurological diseases." Journal of lipid research 55.11 (2014): 2211-2228.
51. Choi, In Young, et al. "A diet mimicking fasting promotes regeneration and reduces autoimmunity and multiple sclerosis symptoms." Cell reports 15.10 (2016): 2136-2146.
52. Steiner, Jennifer L., et al. "Exercise training increases mitochondrial biogenesis in the brain." Journal of applied physiology 111.4 (2011): 1066-1071.
53. Pitceathly, Robert DS, and Carlo Viscomi. "Effects of ketosis in mitochondrial myopathy: potential benefits of a mitotoxic diet." EMBO Molecular Medicine 8.11 (2016): 1231-1233.
54. Ahola, Sofia, et al. "Modified Atkins diet induces subacute selective ragged‐red‐fiber lysis in mitochondrial myopathy patients." EMBO Molecular Medicine (2016): e201606592.
55. Panza, Francesco, et al. "Coffee, tea, and caffeine consumption and prevention of late-life cognitive decline and dementia: a systematic review." The journal of nutrition, health & aging 19.3 (2015): 313-328.
56. Hu, Gang, et al. "Coffee and tea consumption and the risk of Parkinson's disease." Movement disorders 22.15 (2007): 2242-2248.
57. Tremlett, Helen, et al. "The gut microbiome in human neurological disease: A review." Annals of Neurology (2017).
58. Tan, Ai Huey, et al. "Small intestinal bacterial overgrowth in Parkinson's disease." Parkinsonism & related disorders 20.5 (2014): 535-540.
59. Álvarez-Arellano, Lourdes, and Carmen Maldonado-Bernal. "Helicobacter pylori and neurological diseases: Married by the laws of inflammation." World J Gastrointest Pathophysiol 5.4 (2014): 400-404.
60. Pisa, Diana, et al. "Different brain regions are infected with fungi in Alzheimer’s disease." Scientific reports 5 (2015): 15015.
61. de Punder, Karin, and Leo Pruimboom. "Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability." Frontiers in immunology 6 (2015): 223.