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Article ; Online: Myopia, Sodium Chloride, and Vitreous Fluid Imbalance: A Nutritional Epidemiology Perspective.

Brown, Ronald B

Epidemiologia (Basel, Switzerland)

2024 Volume 5, Issue 1, Page(s) 29–40

Abstract: Theories of myopia etiology based on near work and lack of outdoor exposure have had inconsistent support and have not prevented the rising prevalence of global myopia. New scientific theories in the cause and prevention of myopia are needed. Myopia ... ...

Abstract	Theories of myopia etiology based on near work and lack of outdoor exposure have had inconsistent support and have not prevented the rising prevalence of global myopia. New scientific theories in the cause and prevention of myopia are needed. Myopia prevalence is low in native people consuming traditional diets lacking in sodium chloride, and nutritional epidemiological evidence supports the association of rising myopia prevalence with dietary sodium intake. East Asian populations have among the highest rates of myopia associated with high dietary sodium. Similar associations of sodium and rising myopia prevalence were observed in the United States in the late 20th century. The present perspective synthesizes nutritional epidemiology evidence with pathophysiological concepts and proposes that axial myopia occurs from increased fluid retention in the vitreous of the eye, induced by dietary sodium chloride intake. Salt disturbs ionic permeability of retinal membranes, increases the osmotic gradient flow of fluid into the vitreous, and stretches ocular tissue during axial elongation. Based on the present nutritional epidemiology evidence, experimental research should investigate the effect of sodium chloride as the cause of myopia, and clinical research should test a very low-salt diet in myopia correction and prevention.
Language	English
Publishing date	2024-01-29
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-3986
ISSN (online)	2673-3986
DOI	10.3390/epidemiologia5010003
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Can a Low-Phosphate Diet for Chronic Kidney Disease Treat Cancer? An Interdisciplinary Literature Review.

Brown, Ronald B / Bigelow, Philip

Medicines (Basel, Switzerland)

2024 Volume 11, Issue 2

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2024-01-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2777965-8
ISSN	2305-6320
ISSN	2305-6320
DOI	10.3390/medicines11020005
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Salt-Sensitive Hypertension: Mediation by Salt-Induced Hypervolemia and Phosphate-Induced Vascular Calcification.

Brown, Ronald B

Clinical Medicine Insights. Cardiology

2023 Volume 17, Page(s) 11795468231158206

Abstract: Preventing hypertension by restricting dietary salt intake, sodium chloride, is well established in public health policy, but a pathophysiological mechanism has yet to explain the controversial clinical finding that some individuals have a greater risk ... ...

Abstract	Preventing hypertension by restricting dietary salt intake, sodium chloride, is well established in public health policy, but a pathophysiological mechanism has yet to explain the controversial clinical finding that some individuals have a greater risk of hypertension from exposure to salt intake, termed salt-sensitive hypertension. The present perspective paper synthesizes interdisciplinary findings from the research literature and offers novel insights proposing that the pathogenesis of salt-sensitive hypertension is mediated by interaction of salt-induced hypervolemia and phosphate-induced vascular calcification. Arterial stiffness and blood pressure increase as calcification in the vascular media layer reduces arterial elasticity, preventing arteries from expanding to accommodate extracellular fluid overload in hypervolemia related to salt intake. Furthermore, phosphate has been found to be a direct inducer of vascular calcification. Reduction of dietary phosphate may help reduce salt-sensitive hypertension by lowering the prevalence and progression of vascular calcification. Further research should investigate the correlation of vascular calcification with salt-sensitive hypertension, and public health recommendations to prevent hypertension should encourage reductions of both sodium-induced hypervolemia and phosphate-induced vascular calcification.
Language	English
Publishing date	2023-07-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2575256-X
ISSN	1179-5468
ISSN	1179-5468
DOI	10.1177/11795468231158206
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dysregulated phosphate metabolism in autism spectrum disorder: associations and insights for future research.

Brown, Ronald B

Expert reviews in molecular medicine

2023 Volume 25, Page(s) e20

Abstract: Studies of autism spectrum disorder (ASD) related to exposure to toxic levels of dietary phosphate are lacking. Phosphate toxicity from dysregulated phosphate metabolism can negatively impact almost every major organ system of the body, including the ... ...

Abstract	Studies of autism spectrum disorder (ASD) related to exposure to toxic levels of dietary phosphate are lacking. Phosphate toxicity from dysregulated phosphate metabolism can negatively impact almost every major organ system of the body, including the central nervous system. The present paper used a grounded theory-literature review method to synthesise associations of dysregulated phosphate metabolism with the aetiology of ASD. Cell signalling in autism has been linked to an altered balance between phosphoinositide kinases, which phosphorylate proteins, and the counteracting effect of phosphatases in neuronal membranes. Glial cell overgrowth in the developing ASD brain can lead to disturbances in neuro-circuitry, neuroinflammation and immune responses which are potentially related to excessive inorganic phosphate. The rise in ASD prevalence has been suggested to originate in changes to the gut microbiome from increasing consumption of additives in processed food, including phosphate additives. Ketogenic diets and dietary patterns that eliminate casein also reduce phosphate intake, which may account for many of the suggested benefits of these diets in children with ASD. Dysregulated phosphate metabolism is causatively linked to comorbid conditions associated with ASD such as cancer, tuberous sclerosis, mitochondrial dysfunction, diabetes, epilepsy, obesity, chronic kidney disease, tauopathy, cardiovascular disease and bone mineral disorders. Associations and proposals presented in this paper offer novel insights and directions for future research linking the aetiology of ASD with dysregulated phosphate metabolism and phosphate toxicity from excessive dietary phosphorus intake.
MeSH term(s)	Child ; Humans ; Autism Spectrum Disorder ; Central Nervous System ; Autistic Disorder ; Nutritional Status ; Signal Transduction ; Bone Diseases
Language	English
Publishing date	2023-06-13
Publishing country	England
Document type	Journal Article ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/erm.2023.15
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Phosphate toxicity and SERCA2a dysfunction in sudden cardiac arrest.

Brown, Ronald B

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 7, Page(s) e23030

Abstract: Almost half of the people who die from sudden cardiac arrest have no detectable heart disease. Among children and young adults, the cause of approximately one-third of deaths from sudden cardiac arrest remains unexplained after thorough examination. ... ...

Abstract	Almost half of the people who die from sudden cardiac arrest have no detectable heart disease. Among children and young adults, the cause of approximately one-third of deaths from sudden cardiac arrest remains unexplained after thorough examination. Sudden cardiac arrest and related sudden cardiac death are attributed to dysfunctional cardiac ion-channels. The present perspective paper proposes a pathophysiological mechanism by which phosphate toxicity from cellular accumulation of dysregulated inorganic phosphate interferes with normal calcium handling in the heart, leading to sudden cardiac arrest. During cardiac muscle relaxation following contraction, SERCA2a pumps actively transport calcium ions into the sarcoplasmic reticulum, powered by ATP hydrolysis that produces ADP and inorganic phosphate end products. Reviewed evidence supports the proposal that end-product inhibition of SERCA2a occurs as increasing levels of inorganic phosphate drive up phosphate toxicity and bring cardiac function to a sudden and unexpected halt. The paper concludes that end-product inhibition from ATP hydrolysis is the mediating factor in the association of sudden cardiac arrest with phosphate toxicity. However, current technology lacks the ability to directly measure this pathophysiological mechanism in active myocardium, and further research is needed to confirm phosphate toxicity as a risk factor in individuals with sudden cardiac arrest. Moreover, phosphate toxicity may be reduced through modification of dietary phosphate intake, with potential for employing low-phosphate dietary interventions to reduce the risk of sudden cardiac arrest.
MeSH term(s)	Child ; Humans ; Calcium/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Myocardial Contraction/physiology ; Myocardium/metabolism ; Death, Sudden, Cardiac/etiology ; Adenosine Triphosphate
Chemical Substances	Calcium (SY7Q814VUP) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2023-06-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202300414R
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Article ; Online: Biases in COVID-19 Case and Death Definitions: Potential Causes and Consequences.

Brown, Ronald B

Disaster medicine and public health preparedness

2022 Volume 17, Page(s) e313

Abstract: This paper investigates three controversies involving potential causes and consequences of information bias in case and death definitions during the coronavirus disease (COVID-19) pandemic. First, evidence suggests China's surveillance data were biased ... ...

Abstract	This paper investigates three controversies involving potential causes and consequences of information bias in case and death definitions during the coronavirus disease (COVID-19) pandemic. First, evidence suggests China's surveillance data were biased and misinterpreted by the World Health Organization (WHO), prompting the WHO to advise nations to copy China's lockdowns. China appeared to use narrow diagnostic definitions that undercounted cases and deaths. Second, novel genomic data disseminated during the pandemic without adequate guidance from rigorous epidemiologic studies biased infection control policies in many countries. A novel genomic sequence of a virus is insufficient to declare new cases of a novel disease. Third, media reports of COVID-19 surveillance data in many nations appeared to be biased. Broadened surveillance definitions captured additional information, but unadjusted surveillance data disseminated to the public are not true cases and deaths. Recommendations include clarification of the proper use of diagnostic and surveillance case and death definitions to avoid information bias.
MeSH term(s)	Humans ; COVID-19/diagnosis ; COVID-19/epidemiology ; Communicable Disease Control ; SARS-CoV-2 ; Pandemics ; Bias
Language	English
Publishing date	2022-12-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2375268-3
ISSN	1938-744X ; 1935-7893
ISSN (online)	1938-744X
ISSN	1935-7893
DOI	10.1017/dmp.2022.281
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Absolute Risk Reductions in COVID-19 Antiviral Medication Clinical Trials

Ronald B. Brown

Pharmacoepidemiology, Vol 2, Iss 9, Pp 98-

2023 Volume 105

Abstract: COVID-19 antiviral medications approved or authorized for emergency use by the U.S. Food and Drug Administration are reported to have high efficacy in preventing severe illness, hospitalizations, and deaths. However, reports for some of these antivirals ... ...

Abstract	COVID-19 antiviral medications approved or authorized for emergency use by the U.S. Food and Drug Administration are reported to have high efficacy in preventing severe illness, hospitalizations, and deaths. However, reports for some of these antivirals use relative risk reductions from clinical trials without absolute risk reductions. The present paper reappraises recently published clinical trial data for the COVID-19 antivirals paxlovid, remdesivir, and molnupiravir, and reports absolute risk reductions, relative risk reductions, as well as number needed to treat to reduce severe illness, hospitalizations, and deaths. Relative risk reductions are 88.88% for paxlovid (95% CI: 72.13–95.56%), 86.48% for remdesivir (95% CI: 41.41–96.88%), and 30.41% for molnupiravir (95% CI: 0.81–51.18%), while absolute risk reductions are much lower at 5.73% for paxlovid (95% CI: 3.79–7.68%), 4.58% for remdesivir (95% CI: 1.79–7.38%), and 2.96% for molnupiravir (95% CI: 0.09–5.83%). Low absolute risk reductions and the high number of patients needed to treat to reduce severe COVID-19 infections, hospitalizations, and deaths challenge the clinical efficacy of antivirals approved or authorized by the U.S Food and Drug Administration. These findings apply to other populations with similar control event rates. Accurate information should be disseminated to the public when selecting treatments for COVID-19.
Keywords	paxlovid ; remdesivir ; molnupiravir ; COVID-19 antiviral medication ; relative risk reduction ; absolute risk reduction ; Therapeutics. Pharmacology ; RM1-950 ; Other systems of medicine ; RZ201-999 ; Public aspects of medicine ; RA1-1270
Subject code	610
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Body Image, Body Composition, and Aging in Women

Ronald B. Brown

Women, Vol 3, Iss 17, Pp 214-

Insights into an Older Adult Problem

2023 Volume 224

Abstract: Body image is understudied in aging women. The present perspective article reviews body image, body composition, and aging in women. Sarcopenia, a condition of low muscle mass, is associated with aging, and sarcopenia in combination with excessive body ... ...

Abstract	Body image is understudied in aging women. The present perspective article reviews body image, body composition, and aging in women. Sarcopenia, a condition of low muscle mass, is associated with aging, and sarcopenia in combination with excessive body fat causes sarcopenic obesity. Findings of improved health in people with a higher body mass index, known as the obesity paradox, are due to misclassifying healthy people as overweight according to height and body weight instead of according to fat mass and fat-free mass. Body fat infiltrates internal organs in aging adults as increasing levels of body fat are redistributed into the trunk, especially in the abdomen, while subcutaneous fat in the appendages decreases. Accuracy of body image perceptions can determine an individual’s control of body weight. Aging women can protect against sarcopenic obesity by increasing fat-free mass with resistance training and by lowering body fat levels with weight management knowledge and skills. Healthy dietary patterns are low in ultra-processed foods that stimulate excessive consumption of calories and increase body fat levels. In combination with the phosphate additives in ultra-processed food which increase sarcopenia and aging, the present article proposes an etiological pathway in which ultra-processed food consumption eventually leads to aging-related sarcopenic obesity.
Keywords	body image ; body composition ; aging ; women ; sarcopenia ; obesity ; Medicine ; R ; Psychology ; BF1-990
Subject code	796 ; 531
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Cancer Cachexia and Dysregulated Phosphate Metabolism: Insights from Mutant p53 and Mutant Klotho Mouse Models.

Brown, Ronald B

Metabolites

2022 Volume 12, Issue 12

Abstract: The present perspective article proposes that cachexia, muscle wasting in cancer, is mediated by dysregulated phosphate metabolism and phosphate toxicity that can damage tissues in most major organ systems. A diet high in phosphorus fed to mice deficient ...

Abstract	The present perspective article proposes that cachexia, muscle wasting in cancer, is mediated by dysregulated phosphate metabolism and phosphate toxicity that can damage tissues in most major organ systems. A diet high in phosphorus fed to mice deficient in klotho, a cofactor that regulates phosphate metabolism, accelerates aging, sarcopenia, general organ atrophy, kyphosis, and osteoporosis. Similar effects are seen in phenotypes of mutant p53 mice that overexpress the p53 tumor suppressor gene. Although mutant p53 mice do not develop tumors compared to wild-type mice, mutant p53 mice have shorter mean lifespans. Furthermore, tumorigenesis is associated with the sequestration of excessive inorganic phosphate, and dangerous levels of phosphate are released into circulation during tumor lysis syndrome. In total, this evidence implies that tumorigenesis may be a compensatory mechanism that provides protective effects against systemic exposure to dysregulated phosphate metabolism and phosphate toxicity related to cachexia in cancer. Moreover, the hypothetical protection against phosphate toxicity afforded by tumorigenesis also provides an alternate explanation for putative tumor evasion of the immune system. Insights proposed in this perspective paper provide new directions for further research, with potential to develop novel interventions and clinical applications that modify dietary phosphate intake to reduce cachexia in cancer patients.
Language	English
Publishing date	2022-12-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo12121284
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Sudden Infant Death Syndrome, Pulmonary Edema, and Sodium Toxicity: A Grounded Theory.

Brown, Ronald B

Diseases (Basel, Switzerland)

2022 Volume 10, Issue 3

Abstract: Sudden Infant Death Syndrome (SIDS) occurs unexpectedly in an otherwise healthy infant with no identifiable cause of death following a thorough investigation. A general hypervolemic state has been identified in SIDS, and fluid in the lungs suggests the ... ...

Abstract	Sudden Infant Death Syndrome (SIDS) occurs unexpectedly in an otherwise healthy infant with no identifiable cause of death following a thorough investigation. A general hypervolemic state has been identified in SIDS, and fluid in the lungs suggests the involvement of pulmonary edema and hypoxia as the cause of death. The present perspective paper reviews pathophysiological, epidemiological, and dietary evidence in SIDS. A grounded theory is presented that proposes an association of SIDS with sodium toxicity from excessive sodium chloride intake, mediated by noncardiogenic pulmonary edema, hypoxia, and alveolar damage. The peak of SIDS cases occurs in infants 2-4 months of age, who are less efficient in excreting excessive dietary sodium load. Evidence implicating sodium toxicity in SIDS includes increased levels of sodium associated with fever and with inflammatory/immune responses in the lungs. Conditions in near-miss SIDS cases are linked to dysregulated sodium, and increased sodium dietary intake suggests that sodium toxicity from a high-salt diet potentially mediates the association of seasonality and socioeconomic status with SIDS incidence. In addition, exposure to sodium toxicity meets three main criteria of the triple risk model of SIDS. The proposed pathophysiological effects of pulmonary edema related to sodium toxicity in SIDS merit further investigations.
Language	English
Publishing date	2022-08-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720869-2
ISSN	2079-9721
ISSN	2079-9721
DOI	10.3390/diseases10030059
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