Case Report

Resolution of anxiety, binge eating, insomnia, vasomotor symptoms, and laryngopharyngeal reflux with a carnivore ketogenic diet: Case report interpreted through the lens of energy resistance

Moira Newiss

Received: 05 May 2026; Accepted: 29 July 2026; Published: 09 Sept. 2026

Copyright: © 2026. The Author. Licensee: AOSIS.
This work is licensed under the Creative Commons Attribution 4.0 International (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/).

Abstract

This retrospective case report details the resolution of symptoms of lifelong anxiety, panic attacks, binge eating disorder, menopausal vasomotor symptoms, and laryngopharyngeal reflux in a 48-year-old female contemplative scientist. It explores how interventions targeting systemic energy metabolism, consistent with the Energy Resistance Principle and mitochondrial dysfunction, could target the hallmarks of disease. Interventions, including a carnivore ketogenic diet and other lifestyle strategies, are suggested to have improved energy transformation, leading to improvements in symptoms. It is notable that the dietary change resulted in a lean mass hyper-responder lipid profile phenotype, which aligns with an increased reliance on fat metabolism. Compliance with diet is reported using glucose and ketone blood testing, and the qualitative impact is explored from the subject’s perspective.

Keywords: carnivore diet; mitochondrial dysfunction; energy resistance; anxiety; ketogenic diet; vasomotor symptoms; lean mass hyper responder.

Introduction

The Energy Resistance Principle is a framework that describes a new theory on how bioenergetic forces shape health¹. Energy resistance is the property that enables the transformation of energy in the body and the flow of electrons from nutrients towards oxygen in the mitochondria.¹ Cells may be unable to use or respond to energy despite adequate availability, and although some energy resistance is required to sustain life, excess amounts result in reductive and oxidative stress, heat, inflammation, molecular damage, information loss, the hallmarks of disease and ageing.^1,2,3 The framework proposes how lifestyle interventions, including ketogenic diets, sleep, physical activity, and other restorative interventions, promote healing by optimising energy resistance.¹

Many psychiatric disorders share metabolic pathways that contribute to, or exacerbate, psychopathology, including mitochondrial dysfunction, oxidative stress, and inflammation.⁴ The brain has an exceptionally high energy demand, making it especially vulnerable to mitochondrial dysfunction.⁵ Psychosocial stressors, including early life trauma, can disrupt mitochondrial function, impairing energy metabolism, contributing to oxidative stress and inflammation.^6,7

Stress-related diseases are associated with intestinal dysfunction and gut inflammation.^8,9 Oesophageal hypervigilance and symptom-specific anxiety may have a causal role in the development of laryngopharyngeal reflux symptoms.¹⁰ Anxiety, vagal tone, and gastrointestinal motility are interlinked via the brain–gut axis.^8,9,10 Psychological disorders can affect the tight junctions of the oesophageal epithelium and subsequent barrier function, impairing oesophageal motor function and motility, increasing the perception of stimuli via the brain–gut axis.⁹

Menopausal symptoms include vasomotor disturbances (hot flushes and night sweats), fatigue and neuropsychiatric symptoms such as anxiety. These are associated with sympathetic overactivity,^11,12 insulin resistance,¹² and mitochondrial dysfunction.¹³ During perimenopause, declining oestradiol (E2) further worsens this by reducing mitochondrial biogenesis and antioxidant defence, increasing vulnerability to neuroenergetic dysfunction.¹³

The ketogenic diet can improve mitochondrial dysfunction and insulin resistance and reduce inflammation and oxidative stress.^4,14 A state of ketosis has been associated with mood stabilisation and reductions in anxiety.^14,15 Ketogenic diets may help reduce hypersensitised hypothalamic–pituitary–adrenal (HPA) axis responses, dysregulated appetite signalling and food cravings, potentially interrupting addictive feedback loops.^16,17,18 There is some evidence that ketone levels in the blood may correlate with positive changes in daily mood, energy, impulsivity, and anxiety.¹⁵ Complete remission of major depression and generalised anxiety disorder has been reported to occur within 7–12 weeks of nutritional ketosis.¹⁵ There are two case reports of remission of binge eating, and three case reports of remission of anxiety disorder, using a ketogenic diet.^19,20 While there are no trials or case reports of ketogenic diets in relation to vasomotor symptoms these symptoms are thought to originate in the thermoregulatory centre of the hypothalamus, one of the most energy-sensitive regions in the body, suggesting high mitochondrial activity to maintain stable signalling.

A strict carnivore ketogenic diet is purely made up of meat and animal fat and devoid of any plant foods.²¹ This case report details that implementation of a carnivore ketogenic diet alongside other lifestyle strategies resulted in the reduction, and in some cases remission, of a range of symptoms including anxiety and binge eating behaviours, reflux, insomnia, and hot flushes.

Case presentation

Clinical background

The subject was a 48-year-old single, peri-menopausal female, living alone, spending a large part of her day engaged in meditative activities. She had ceased menses for several months. Her body mass index (BMI) was 21, current weight 46 kg, height 148 cm, no recent medication, no caffeine, alcohol, or nicotine use. No recent blood work was available.

The subject had struggled with a sense of fear and worry for many years despite psychological therapy. In her teenage years, binge eating behaviours developed after use of a calorie-controlled diet and continued throughout life, overconsuming foods such as chocolate, dried fruit, and oat-based products. She reported feeling anxious, worried, agitated, tired, fearful, daily panic attacks, intrusive thoughts, and heart palpitations. The mental health symptoms, including the binge eating behaviours, intensified 2 years ago on entering a lengthy meditation retreat, when she had a constant desire to binge on sweet and salty foods. She experienced no quieting of the mind, making it difficult to meditate effectively.

The subject had long-term gastrointestinal issues starting 8 years previously when eating a vegan diet, worsening with a raw vegan diet. Symptoms included heartburn, pain, post-nasal drip, excessive phlegm, burping after meals, and being unable to drink for up to 6 h after eating, all consistent with a previous diagnosis of laryngopharyngeal reflux. She reported undigested food in stools, bloating, nausea, and loose stools. Seven years previously, a diagnosis of diverticulitis and Helicobacter pylori was successfully treated with antibiotics. She reported peri-menopause symptoms including insomnia, hot flushes (5 times a day and 6 times a night) alongside regular mood swings. She was fatigued and drowsy during the day. In addition, she experienced back pain and ovarian cysts.

The subject was taking a self-prescribed blend of black pepper, pippali and ginger; 5000 IU of vitamin D; 200 mg of vitamin K daily; porcine pancreatic enzymes; a gastrointestinal repair formula; magnesium; electrolytes; iodine; diindolylmethane; and calcium d-glucarate.

Despite trying all sorts of diets, supplements, and psychological support, the subject was still desperate to feel well again. Her goal was to calm her mind so she could meditate effectively, resolve gut problems, improve sleep, and reduce hot flushes.

Intervention strategy to minimise energy resistance

At the first consultation with the nutritional therapy practitioner, the subject was eating a breakfast of ground beef with tallow or liver in butter, a lunch of salad with avocado, eggs, olive oil, and apple cider vinegar, and dinner comprising salmon cooked in ghee or a feta cheese salad. She was drinking one and a half litres of water a day as well as bone broth. She spent most of the day lying down to limit back pain and was able to manage a short evening walk.

It was agreed in Week 1 that the subject would adopt a pure carnivore meat and animal fat ketogenic diet, avoiding all plant products, serving as a nutrient-dense elimination diet. The food was beef cooked in animal fat, with salt added to taste. The aim was to implement a 2:1 ratio of fat to protein and a protein intake of 1.5 g/kg of ideal body weight, equating to 56 g a day. It was recommended to include liver a couple of times a week, a daily cup of bone broth, and some bone marrow. Example meals were provided, including rib-eye steak with added beef tallow.

It was recommended to move the last meal forward to allow her digestive system 3 h to process food before bed. In addition, it was suggested to slowly increase her movement during the day with gentle stretches and a second daily walk, as well as keeping lights dimmed before bed to promote sleep and support circadian alignment. Supplements were stopped except the pancreatic enzyme, vitamin D 5000 IU per day, K2 200 mcg per day, and iodine 2% 4 drops per day. The rationale was to simplify supplementation and eliminate anything potentially contributing to symptoms; the enzyme support was continued as compromised digestion was suspected, vitamin D and K2 because of a lack of adequate exposure to natural light, and iodine as it may be supportive in reducing ovarian cysts.

It was advised to check blood glucose and beta-hydroxybutyrate (BHB) ketones once a day before dinner, at least 3–4 h after last eating. The aim was to get ketones (BHB) between 2 mmol/L and 3.5 mmol/L. During initial transition into ketosis, the subject experienced a worsening of anxiety symptoms, with a couple of nights with intense panic attacks lasting 30 min, followed by a strong desire to consume food. This resolved within a few days and was possibly due to increased physiological stress during metabolic adaptation. The subject quickly achieved ketone (BHB) levels of between 2 mmol/L and 4 mmol/L and blood glucose between 3.5 mmol/L and 5.5 mmol/L. In Week 2, the subject reported feeling better; reflux symptoms had reduced with only an occasional burping and burning sensation, although she still experienced loose stools. She was now able to drink fluids after a meal, which had previously been impossible. She felt food was no longer sitting in her stomach for hours. Energy was good, and although sleep was still a little disrupted, no longer drowsy during the day. The biggest benefit was that during the day her mind was calm and still, and she was no longer constantly hungry or craving sweet food. Her hot flushes were also much reduced during the day, to the point that she almost forgot about them, with a few more at night and a little anxiety, plus she had experienced two particularly bad panic attacks.

At Week 6, the subject visited relatives and reintroduced some vegetables including lettuce, avocado, courgette and pepper; her level of ketones (BHB) dropped down to between 0.4 mmol/L and 0.5 mmol/L ketones (BHB) while glucose remained steady between 3.5 mmol/L and 5.5 mmol/L. This experiment resulted in her feeling worse, with reflux symptoms and anxiety returning. She had her blood lipids (see quantitative analysis) and vitamin D tested; the latter was optimal (61 ng/mL) so supplementation was stopped.

Once home again (Week 7), she resumed the carnivore ketogenic diet now consisting of beef, lamb, and butter as well as liver, bone broth, and bone marrow. Butter was introduced to swap out the beef tallow, which was felt to be causing diarrhoea, and this helped firm up the stool. Again, whilst transitioning back to a higher level of ketosis, she experienced more severe anxiety and panic attacks and was constantly woken at night by anxiety and hot flushes. This resolved within a few days.

At her last consultation (Week 12) with the nutritional therapy practitioner, the subject reported feeling very good. Her ketones (BHB) remained around the 2 mmol/L – 3.5 mmol/L level. The diet had been broadened to include some fish and other organ meat, now consisting of beef, lamb, sardines, and salmon with butter plus some liver, heart, lungs and bone marrow. Her energy was great, and sleep was much improved with only an occasional waking during the night. Her mind was constantly still and calm. Reflux was much better, with an occasional burning sensation. Hot flushes had disappeared during the day with an occasional small one at night—no sign of any binge eating behaviours or late-night eating. Back pain had improved enough for her to walk for 1 h a day. At no point over the 12 weeks did the client report needing to access psychological therapy support.

The timeline below (Table 1) sets out the key points relating to consultations with the nutritional therapy practitioner.

Quantitative analysis

The subject remained in ketosis for 3 months, mostly between 2 mmol/L and 3.5 mmol/L ketones (BHB), with a short deviation to a lower level whilst abroad, confirmed with daily blood testing (Figure 1). The subject remained weight stable. Hot flushes reduced from 5 times a day and 6 times a night to 0 during the day, with only an occasional one at night. Panic attacks reduced from daily to zero. She was now able to drink water any time after eating.

FIGURE 1: Monitoring of blood glucose and ketones over 3 months.

At Week 6, a metabolic health blood panel was completed. The results met the published criteria for a lean mass hyper-responder (LMHR) phenotype with low-density lipoprotein (LDL) 345 mg/dL, high-density lipoprotein (HDL) 118 mg/dL, triglycerides (TG) 64 mg/dL (see Table 2).²² Total cholesterol/HDL ratio of 4 and a TG/HDL ratio of 0.5. However, as no baseline results were available prior to starting the diet, it cannot be confirmed that this occurred following introduction of the diet or reflected a pre-existing lipid profile diet. Based on case reports, this pattern was not unexpected^22,23, and current research regarding the LMHR phenotype was discussed with the subject, who remained happy to continue the diet, declining any further testing such as a coronary calcium computed tomography scan or onward referral to a cardiologist.

The lipid profile met the published criteria for the LMHR phenotype. However, as baseline lipid measurements prior to commencing the ketogenic diet were unavailable, it cannot be determined whether this phenotype developed in response to the dietary intervention or reflected the participant’s pre-existing lipid profile. Furthermore, although the LMHR phenotype has been described in lean individuals consuming carbohydrate-restricted diets, current cardiovascular guidelines continue to regard elevated low-density lipoprotein cholesterol (LDL-C) as a potential risk factor for atherosclerotic cardiovascular disease, and the long-term clinical implications of the LMHR phenotype remain uncertain.

Qualitative analysis

The client scored three symptoms to help track the impact of the lifestyle interventions (see Table 3). This showed significant changes with reflux, insomnia and hot flushes all improving by several points on the scale.

The subject reported at Week 12 that all her symptoms were much better, and her energy had returned. She felt ‘cutting carbohydrates helped but things improved even more on the carnivore ketogenic diet, then the panic attacks then stopped completely’. It was now normal for her mind to be calm and still, ‘I feel great in my mind, there is stillness and clarity and all the strange, self-deprecating, or negative thoughts have gone away’. This enabled her to meditate more effectively, which was important to her. She no longer had food cravings, nor did she experience any binge eating behaviours.

Hot flushes were much reduced, and she was sleeping very well. Regarding laryngopharyngeal reflux, she reported being able to drink water straight after a meal, the post-nasal drip had resolved completely, and her digestive system felt like it was working properly with no burping, bloating, or nausea.

The subject found the diet a little monotonous but did not want to go back to a vegetarian style of eating, suspecting it would result in recurrence of binge eating behaviours. She was happy with the outcome and planned to continue eating a slightly more liberal animal-based ketogenic diet, hoping for even more improvements over the coming months.

Discussion

The hallmarks of disease (see Table 4) contribute to and are associated with mitochondrial dysfunction.^1,2,3 The improvements seen across psychological, gastrointestinal, and vasomotor symptoms may share common roots involving deregulated nutrient sensing, dysregulated HPA axis activity and altered brain–gut communication, oxidative stress, inflammation, altered intercellular communication, and circadian rhythm dysregulation, all of which theoretically increase energy resistance. It is hypothesised that these disease processes are reversed due to the synergistic effect of the ketogenic diet along with other lifestyle and restorative interventions, including physical activity and meditation, which acted to support mitochondrial function, optimise energy resistance, and promote healing.^1,6

The body of evidence suggesting that a carnivore version of the ketogenic diet has therapeutic potential is small and more research is needed. The elimination of plant foods may be significant, reducing exposure to dietary antigens, anti-nutrients, and fibre, which have been linked to immune or gastrointestinal disturbances in sensitive individuals,²⁵ all potential sources of energy resistance. A carnivore diet may provide a highly bioavailable source of nutrients, helping address any potential nutrient deficiencies^21,26, helping optimise energy resistance.

The strengths of this case report include that compliance with the diet was measured with ketone (BHB) and glucose levels. As a contemplative scientist, the subject’s state of mind was of huge importance, and she was highly motivated to make significant changes; this could have increased bias in outcomes. Limitations include that no validated scales were used to measure improvements in symptoms and, as a result, are anecdotal and subject to recall, confirmation, and placebo effect biases. It could be argued that there is a significant confounding aspect to this case because multiple things changed at once: diet composition, meal timing, activity recommendations, sleep-light hygiene; but through a lens of energy resistance, this is expected. In addition, supplements changed; some stopped; some continued; some discontinued later. It is difficult to know what impact they had compared to the other therapies. The quasi-experiment where plant foods were reintroduced, and symptoms returned, also had confounding elements due to travel and psychosocial interactions.

There is a lack of research on carnivore ketogenic diets; there are no controlled trials in the literature. Research investigating the nutrient content of carnivore diets reports mixed results with possible deficiencies²¹, although studies of individuals consuming a carnivore diet do not demonstrate negative effects.^27,28 Deficiencies from meal planning analysis suggest carnivore diets may be below the recommended daily intake for: thiamine, magnesium, calcium, Vitamin C, iron, folate, and iodine, depending on foods included in the diet.²¹ This suggests that although a carnivore diet can be therapeutic in the short term, it may be necessary to increase the variety of foods consumed long term, and testing for deficiency should be strongly considered.

One concern regarding ketogenic diets is their high fat content in relation to cardiovascular disease, with high LDL-C seen as an independent risk factor.²⁹ A 2025 review found that a reduction in saturated fats could not be recommended to prevent cardiovascular disease and mortality³⁰, which aligns with a previous review finding no evidence of a link between fat intake and risk of coronary heart disease or cardiovascular disease mortality.³¹ Raised LDL-C levels can occur in a subset of individuals on a ketogenic diet, the LMHR phenotype^22, who are deemed to be lean (BMI of < 25 kg/m²) and have elevated high-density lipoprotein cholesterol (HDL-C) and low TG, generally healthy.²² High LDL-C more than 500 mg/dL does not always associate with increased plaque burden³², questioning the absolute risk associated with the LMHR phenotype. The theory presented to explain this phenotype is known as the Lipid Energy Model, where lean metabolically healthy individuals on a ketogenic diet have increased very low-density lipoprotein (VLDL) secretion, TG hydrolysis, and VLDL turnover, presenting as a profile of low TG, elevated HDL-C, and elevated LDL-C.²² The model predicts that the rate of lipoprotein lipase (LPL) mediated VLDL turnover relates to energy demands and inversely relates to body fat mass.²² However, the long-term cardiovascular implications of the LMHR phenotype remain uncertain, and further research is warranted to properly characterise the risk associated with this unique metabolic profile, including controlled clinical trials and studies with longer durations. Recommended follow-up might include testing apolipoprotein B (ApoB), Lp(a) and low-density lipoprotein particle number (LDL-P) if available, blood pressure tracking, appropriate imaging, and a cardiology consultation.

Several mechanisms may potentially explain the improvement in vasomotor symptoms observed with a ketogenic diet, leading to enhanced hypothalamic function, including improved energy metabolism, reduced neuroinflammation, improved insulin sensitivity and metabolic flexibility, modulation of autonomic nervous system activity, and altered neurotransmitter signalling.^11,12,33 Together, it is hypothesised that these effects may help restore thermoregulatory homeostasis during the menopausal transition.

Conclusion

This case report describes the resolution of multiple symptoms including fatigue, anxiety, insomnia, binge eating behaviours, hot flushes, and reflux in a perimenopausal subject following a combined dietary and lifestyle intervention focused on a carnivore ketogenic diet alongside circadian alignment, movement, and meditation practices. It is explored from a bioenergetic view of disease where impaired energy transformation, particularly in high-demand tissues including the brain, leads to the inability of cells and tissues to maintain organised and regulated function, leading to disease. The combined lifestyle interventions aimed to tackle the hallmarks of disease and likely all contributed to optimise energy resistance.

The energy resistance framework hypothesises that cells may exhibit a reduced capacity to use or respond to available energy, despite adequate substrate availability. In contrast, the Lipid Energy Model describes how the body mobilises and transports fuel in the form of lipids when carbohydrates are restricted. Viewed together, this case may reflect a shift in whole-body bioenergetics in terms of energy availability, distribution, and cellular utilisation. It is possible that the observed clinical improvements may be due to improving both fuel availability and energy transformation and delivery mechanisms. As a single case study, this report highlights how the lens of energy resistance may help develop personalised integrative therapeutic lifestyle strategies.

Acknowledgements

The author declares that no financial or personal relationships inappropriately influenced the writing of this article.

Moira Newiss: Writing – original draft, Writing – review & editing. The author confirms that this work is entirely their own, has reviewed the article, approved the final version for submission and publication, and takes full responsibility for the integrity of its findings.

Written informed consent was obtained from the individual for the publication of the data included in this article.

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

The author confirms that the data supporting the findings of this study are available within the article.

The views and opinions expressed in this article are those of the author and are the product of professional research. They do not necessarily reflect the official policy or position of any affiliated institution, funder, agency, or that of the publisher. The author is responsible for this article’s results, findings, and content.

References