The Role of Nutrition and Physical Activity as Trigger Factors of Paralytic Attacks in Primary Periodic Paralysis
Open accessAbstract
Background: Primary periodic paralysis (PPP) are rare inherited neuromuscular disorders including Hypokalemic periodic paralysis (HypoPP), Hyperkalemic periodic paralysis (HyperPP) and Andersen-Tawil syndrome (ATS) characterised by attacks of weakness or paralysis of skeletal muscles. Limited effective pharmacological treatments are available, and avoidance of lifestyle related triggers seems important. Objective: Our aim was to search and assess the scientific literature for information on trigger factors related to nutrition and physical activity in PPP. Methods: We searched Ovid Medline and Embase database for scientific papers published between January 1, 1990, to January 31, 2020. Results: We did not identify published observation or intervention studies evaluating effect of lifestyle changes on attacks. Current knowledge is based on case-reports, expert opinions, and retrospective case studies with inadequate methods for description of nutrition and physical activity. In HypoPP, high carbohydrate and salt intake, over-eating, alcohol, dehydration, hard physical activity, and rest after exercise are frequently reported triggers. Regarding HyperPP, fasting, intake of potassium, alcohol, cold foods or beverages, physical activity, and rest after exercise are frequently reported triggers. No nutrition related triggers are reported regarding ATS, exercise can however induce ventricular arrhythmias. Conclusions: Our results support that dietary intake and physical activity may play a role in causing paralytic attacks in PPP, although the current scientific evidence is weak. To provide good evidence-based patient care, several lifestyle aspects need to be further assessed and described.
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Insulin has been reported to reduce the conductance of inward-rectifier potassium (Kir) channels, which may impair potassium re-equilibration across the membrane.
“Additionally, insulin has been reported to reduce the conductance of inward-rectifier potassium (Kir) channels, which may impair potassium re-equilibration across the membrane [31].”
From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [31]
The Discussion (page not provided) reports a proposal that insulin reduces inward-rectifier potassium conductance in hypokalemic periodic paralysis patients and a potassium-depleted rat model. It links this to membrane depolarization, but does not say that potassium re-equilibration across the membrane is impaired; the claim also omits the populations to which the proposal applies. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe post-exercise insulin surge can lead to abrupt hypokalemia and paralysis in susceptible individuals.
“This post-exercise insulin surge can lead to abrupt hypokalemia and paralysis in susceptible individuals [31].”
From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [31]
The Introduction says that post-exercise potassium shifts or insulin administration can cause hypokalemia, while the Discussion links insulin-driven potassium shifts to possible paralysis in susceptible patients. Neither section describes a post-exercise insulin surge; the Discussion instead associates an insulin spike with carbohydrate intake and says the proposed pathway to paralysis lacks evidence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredDuring physical activity, potassium is released from skeletal muscle into the plasma to support muscle contraction, and in the recovery phase, insulin secretion rises to promote glycogen repletion and drives potassium reuptake into muscle cells.
“During physical activity, potassium is released from skeletal muscle into the plasma to support muscle contraction. In the recovery phase, insulin secretion rises to promote glycogen repletion and also drives potassium reuptake into muscle cells.”
From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [31]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredProlonged depolarization of the sarcolemma leads to sustained sodium channel inactivation, inhibiting action potential generation and rendering muscle fibers electrically unexcitable.
“Prolonged depolarization of the sarcolemma leads to sustained sodium channel inactivation, inhibiting action potential generation and rendering muscle fibers electrically unexcitable [31].”
From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [31]
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Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms
Qing, G., Zakaria, W. N. A., Rom, F. Z. M., Nik, W. N. F. H. W., Zulkeflee, H. A., & Rahim, S. N. A. (2025) · Endocrinology and Metabolism · doi:10.3803/enm.2025.2554 · Cited by 5 · see citing works
“This activates Na + /K + -ATPase, further enhancing the intracellular shift of potassium [31].”
Influential
- Authors
- Welland, N. L., Hæstad, H., Fossmo, H. L., Giltvedt, K., Ørstavik, K., & Nordstrøm, M.
- Affiliations
- Frambu Resource Centre for Rare Disorders (Frambu), Siggerud, Norway
- University Hospital of North Norway (NO)
- Oslo University Hospital (NO)
- Corresponding author
- Welland, Natasha Lervaag
- Venue
- Journal of Neuromuscular Diseases
- Publisher
- SAGE Publications
- Published
- 2021-02-24
- Volume
- 8
- Issue
- 4
- Pages
- 457-468
- ISSN
- 2214-3599 (ISSN-L)
- 2214-3602
- PMC
- PMC8385530
- OpenAlex
- W3134788189
- Cited by
- 14
- References
- 36
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 4 · 2022: 2
- FWCI
- 0.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuromuscular Diseases (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Universitetet i Oslo
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- hypokalemic periodic paralysis, hyperkalemic periodic paralysis, Andersen-Tawil syndrome, precipitating factors, nutrition, physical activity, dietary intake, lifestyle modification
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Diet, Female, Humans, Male, Middle Aged, Paralysis, Paralyses, Familial Periodic, Exercise, Andersen Syndrome, Young Adult
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