Evidence map›Paper›PMID 26693381›Full record

ReviewInternational journal of evolutionary biology2015

An Evolutionary Perspective of Nutrition and Inflammation as Mechanisms of Cardiovascular Disease.

María Esther Rubio-Ruiz, Ana Elena Peredo-Escárcega, Agustina Cano-Martínez, Verónica Guarner-Lans

Open access · hybridAbstract readReview
In one paragraph

Review in International journal of evolutionary biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 43 citations in OpenAlex.

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  13. [Evolutionary cardiology and experimental research].Archivos de cardiologia de Mexico · 2022
    Article
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  16. Healthy cardiovascular biomarkers across the lifespan in wild-born chimpanzees (Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

María Esther Rubio-RuizDepartment of Physiology, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Mexico City, DF, Mexico.
Ana Elena Peredo-EscárcegaDepartment of Physiology, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Mexico City, DF, Mexico.
Agustina Cano-MartínezDepartment of Physiology, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Mexico City, DF, Mexico.
Verónica Guarner-LansDepartment of Physiology, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Mexico City, DF, Mexico.
Instituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When cardiovascular diseases are viewed from an evolutionary biology perspective, a heightened thrifty and an inflammatory design could be their mechanisms. Human ancestors confronted a greater infectious load and were subjected to the selection for proinflammatory genes and a strong inflammatory function. Ancestors also faced starvation periods that pressed for a thrifty genotype which caused fat accumulation. The pressure of sustaining gluconeogenesis during periods of poor nourishment selected individuals with insulin resistance. Obesity induces a proinflammatory state due to the secretion of adipokines which underlie cardiometabolic diseases. Our actual lifestyle needs no more of such proinflammatory and thrifty genotypes and these ancestral genes might increase predisposition to diseases. Risk factors for atherosclerosis and diabetes are based on inflammatory and genetic foundations that can be accounted for by excess fat. Longevity has also increased in recent times and is related to a proinflammatory response with cardiovascular consequences. If human ancestral lifestyle could be recovered by increasing exercise and adapting a calorie restriction diet, obesity would decrease and the effects on chronic low-grade inflammation would be limited. Thereby, the rates of both atherosclerosis and diabetes could be reduced.

Identifiers

PMID26693381
PMCPMC4677015
OpenAlexW2199279306

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.