Categories:

Body Temperature, Metabolism, and Obesity

Also see:
Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH
Temperature and Pulse Basics & Monthly Log
Thyroid, Temperature, Pulse
Is 98.6 Really Normal?
Metabolism, Brain Size, and Lifespan in Mammals
Promoters of Efficient v. Inefficient Metabolism
Inflammation from Decrease in Body Temperature
Melatonin Lowers Body Temperature
Menopausal Estrogen Therapy Lowers Body Temperature
Thyroid Function, Pulse Rate, & Temperature
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase

Metabolism. 2009 Jun;58(6):871-6. doi: 10.1016/j.metabol.2009.02.017.
Is obesity associated with lower body temperatures? Core temperature: a forgotten variable in energy balance. (full paper)
Landsberg L, Young JB, Leonard WR, Linsenmeier RA, Turek FW.
The global increase in obesity, along with the associated adverse health consequences, has heightened interest in the fundamental causes of excessive weight gain. Attributing obesity to “gluttony and sloth”, blaming the obese for overeating and limiting physical activity, oversimplifies a complex problem, since substantial differences in metabolic efficiency between lean and obese have been decisively demonstrated. The underlying physiological basis for these differences have remained poorly understood. The energetic requirements of homeothermy, the maintenance of a constant core temperature in the face of widely divergent external temperatures, accounts for a major portion of daily energy expenditure. Changes in body temperature are associated with significant changes in metabolic rate. These facts raise the interesting possibility that differences in core temperature may play a role in the pathophysiology of obesity. This review explores the hypothesis that lower body temperatures contribute to the enhanced metabolic efficiency of the obese state.

Some quotables:

“Resting (or “basal”) metabolic rate (RMR) accounts for
approximately 80%of energy output. About two thirds of RMR
is for maintenance of homeothermy (warm-bloodedness); about
one third is to maintain cellular integrity, ionic gradients, protein
turnover, and the like [6-8] Resting metabolic rate is largely
regulated by thyroid hormones, with a minor contribution from
the sympathetic nervous system. Resting metabolic rate differs
by as much as 600 kcal/d for a 70-kg man [8].
Physical activity (exercise) accounts for about 10% in
truly sedentary humans; in addition to intentional activity,
this category includes nonpurposeful motion such as
fidgeting, which may differ among lean and obese
individuals [9], as well as upright posture [10].
The remaining 10% is frequently referred to as thermogenesis,
which means heat production unrelated to physical
activity.”

“It should be emphasized that, for nonsedentary individuals,
the activity component may be much greater than 10%
of total energy expenditure. Evidence has been developed
indicating that the combination of activity plus adaptive
thermogenesis accounts for about 44% of total energy
expenditure on average, meaning that RMR would constitute
about 56% of total energy expenditure in normally active
humans [15], as compared with 80% in the truly sedentary.”

“A lesser ability to dissipate ingested calories is one
example of a thrifty metabolic trait that has evolved to
promote survival in the face of fluctuations in food
availability. Since the initial formulation of the “thrifty
gene” hypothesis by James Neel in 1962 [16], the nature of
thrifty traits has been the subject of considerable research
and speculation. A recent formulation [17] highlights 2
distinct components: (1) decreased metabolic rate and/or a
diminished capacity for “thermogenesis” and (2) decreased
insulin sensitivity. These 2 components address the 2 main
physiologic imperatives of starvation: energy conservation
and protein preservation. A decrease in metabolic rate would
lead to more efficient storage of calories as fat, thereby
prolonging survival during famine; during periods of
abundance and in the face of dietary excess, this trait
would predispose to obesity. Resistance to the action of
insulin would divert glucose from skeletal muscle, which can
use fat-derived substrates, to the brain, an organ almost
entirely obligated to the use of glucose. In the presence of
famine, insulin resistance would spare muscle breakdown by
lessening the need for gluconeogenesis from protein; in the
face of an abundant food supply, however, and in association
with dietary excess, insulin resistance would predispose to
type 2 diabetes mellitus.”

“Both metabolic efficiency and insulin resistance, moreover,
are known to vary among different individuals in the
same population. The survival value of these thrifty traits,
embedded in our genome by natural selection, underlies the
current epidemic of obesity and type 2 diabetes mellitus. The
ravages of obesity in once lean indigenous peoples, such as
the Pima Indians of the US southwest [18,19], the Aboriginal
peoples of Australia [20,21], and the Maoris of New Zealand
[22], exemplify the maladaptive side of these thrifty traits in
the presence of an abundant high-energy food supply.”

“The prime importance of energy conservation is demonstrated
by the decline in metabolic rate that occurs during
starvation, a response that involves suppression of sympathetic
nervous system (SNS) activity [23]. Body temperature
also falls [24]. This conservative response that limits weight
loss during starvation also diminishes the efficacy of low energy
diets in the treatment of obesity [12,14].”

“Approximately two thirds of RMR is expended in
meeting the requirement of homeothermy [6,7], the maintenance
of a constant body temperature of about 37°C
(98.6°F). In truly sedentary humans where RMR is 80% of
total energy expenditure, this means that more than 50% of
total energy expenditure is dedicated to maintaining this
constant core temperature. In normally active humans where
the RMR accounts for 56% of total energy expenditure [15],
approximately 37% of total energy output is expended in the
maintenance of homeothermy. This impressive contribution
that warm-bloodedness makes to overall energy production
is exemplified by the difference in energy output between
poikilotherms and homeotherms; a mouse has a many fold
greater metabolic rate than a lizard of the same weight [37].
This metabolic energy required for homeothermy is thyroid
dependent and apparently generated principally in mitochondria
throughout the body of warm-blooded animals. The
adaptive forms of thermogenesis, in contrast, are regulated
by the sympathetic nervous system and generated, at least in
part, in brown adipose tissue (BAT) [38]. It is of interest that
recent observations using positron emission tomographic
scanning have resuscitated interest in functional BAT in adult
humans [39,40].

The important relationship of body temperature to
metabolic rate is also demonstrated by the effect of
temperature elevation on the rate of oxygen consumption.
Raising core temperature by 1°C is associated with a 10% to
13% increase in metabolic rate [41]. During starvation, a fall
in body temperature occurs, contributing to the decrease in
metabolic rate noted in this state [24]. Are differences in
body temperature responsible for interindividual variations
in RMR? Is it possible that the obese have a lower body
temperature than normal-weight persons? Or that, during
periods of low energy intake or during sleep, the obese have
an exaggerated fall in temperature? Good data appear to be
lacking; a recent book on energy metabolism and obesity
[42], for example, fails to even mention a potential role for
core temperature. Body temperature in the obese is clearly
worthy of study given the overriding importance of core
temperature as the major factor in energy expenditure.”

“Parenthetically, measurements
of core temperature can be made precisely and
are free of the conundrum imposed by differences in body
size because core temperature is regulated centrally for the
whole body.”

“10. Is core temperature lower in the obese?

Lowering body temperature is an established strategy
used by homeotherms to conserve energy. Some animal
models of obesity, including the obese (ob/ob) mouse
[52,53] and the Zucker fatty (fa/fa) rat [54], are
hypothermic compared with lean controls. Hibernation
and the lesser state of shallow torpor wherein the
temperature falls at night are energy-saving adaptations
used by a variety of mammals [55,56] and even some
human populations such as the Australian Aboriginals
[57]. A decrease in body temperature, in fact, occurs at
night in relation to the sleep cycle in human populations
[58,59]. A fall in body temperature occurs during
starvation, as noted above, and in hypoglycemia, an
acute state of energy deprivation [60-62]. Recent evidence
implicating fibroblast growth factor 21 in the metabolic
response to fasting supports the important adaptive role
that temperature plays in the adaptation to starvation. In
addition to stimulating lipolysis, fibroblast growth factor
21 lowers temperature and induces torpor [63]. Lower
temperature has also been linked to obesity in mice with
BAT ablation [64].”

“11. Quantitative significance of changes in
core temperature

Some quantitative considerations, although crude, also
serve to demonstrate the potential importance of core
temperature. A positive balance of 3500 to 4000 kcal
results, theoretically, in the deposition of 1 lb of fat.
Walking 1 mile, a normal-sized individual burns about 100
kcal, the amount of energy contained in 10 potato chips
and equivalent to 5% of a total energy intake of 2000 kcal/
d. A 1°C increase in core temperature, by comparison,
would increase metabolic rate by 10% to 13% [41]. In the
example of extreme sedentary existence cited above where
metabolic rate approximates 50% of overall energy output
(or about 1000 kcal for a normal-sized person), a 1°C
increase in core temperature increases expenditure of 100
to 130 kcal/d. Such an individual could achieve energy
balance eating 100 to 130 kcal more per day than one with
a 1.0°C lower body temperature. Individuals with the 1°C
lower core temperature, thus, would have a thermogenic
handicap of about 100 to 130 kcal/d or about 3000 to 4000
kcal/mo. In 1 month, this would account for 1 lb of fat, 12
lb in 1 year, and about 120 lb in a decade, all else being
equal. In the normally active example described above
where RMR constitutes 37% of total energy expenditure,
the impact is less but still impressive. Under these
circumstances, the thermogenic handicap of a 1°C lower
core temperature might approximate 74 to 96 kcal/d or
about 2200 to 2900 kcal/mo. Greater falls in temperature,
perhaps during sleep or in response to low-energy diets,
would have correspondingly greater effects.

12. Summary

Given the importance of RMR in overall energy output
and the importance of homeothermy as the major component
of RMR, core temperature should be evaluated as a potential
cause of individual differences in metabolic efficiency in
humans. Assessing core temperature in the obese can be
done, furthermore, without the confounding need to normalize
energy expenditure per unit of body mass. In these
studies, assessment of core temperature should be done for
prolonged periods, should sample day and night temperatures,
and should assess the impact of fasting and low energy
intake on obese and lean individuals. Cross-sectional, and
especially longitudinal, population-based studies could
define the role of core temperature in the pathogenesis of
obesity. Information gained in such studies, along with
research into the central nervous system regulation of
temperature set point and the regulation of mitochondrial
metabolism, might enable the development of new therapeutic
strategies designed to enhance energy output.“

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By Team FPS – January 5, 2013

Sugar Ads

Also see:
Gelatin Ads
Polyunsaturating America: Mazola’s Marketing
















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By Team FPS – December 30, 2012

Cheese making dates back 7500 years

Also see:
Cheese Chunks Adorn Ancient Mummies
Calcium Paradox
Hypertension and Calcium Deficiency
Blood Pressure Management with Calcium & Dairy
Calcium to Phosphorus Ratio, PTH, and Bone Health
Low CO2 in Hypothyroidism
Fatty Acid Synthase (FAS), Vitamin D, and Cancer
Parmigiano Reggiano cheese and bone health
Source of Dietary Calcium: Chicken Egg Shell Powder
Milk in context: allergies, ecology, and some myths

Nature (2012) doi:10.1038/nature11698
Earliest evidence for cheese making in the sixth millennium bc in northern Europe
Mélanie Salque, Peter I. Bogucki, Joanna Pyzel, Iwona Sobkowiak-Tabaka, Ryszard Grygiel, Marzena Szmyt & Richard P. Evershed
The introduction of dairying was a critical step in early agriculture, with milk products being rapidly adopted as a major component of the diets of prehistoric farmers and pottery-using late hunter-gatherers1, 2, 3, 4, 5. The processing of milk, particularly the production of cheese, would have been a critical development because it not only allowed the preservation of milk products in a non-perishable and transportable form, but also it made milk a more digestible commodity for early prehistoric farmers6, 7, 8, 9, 10. The finding of abundant milk residues in pottery vessels from seventh millennium sites from north-western Anatolia provided the earliest evidence of milk processing, although the exact practice could not be explicitly defined1. Notably, the discovery of potsherds pierced with small holes appear at early Neolithic sites in temperate Europe in the sixth millennium BC and have been interpreted typologically as ‘cheese-strainers’10, although a direct association with milk processing has not yet been demonstrated. Organic residues preserved in pottery vessels have provided direct evidence for early milk use in the Neolithic period in the Near East and south-eastern Europe, north Africa, Denmark and the British Isles, based on the δ13C and Δ13C values of the major fatty acids in milk1, 2, 3, 4. Here we apply the same approach to investigate the function of sieves/strainer vessels, providing direct chemical evidence for their use in milk processing. The presence of abundant milk fat in these specialized vessels, comparable in form to modern cheese strainers11, provides compelling evidence for the vessels having being used to separate fat-rich milk curds from the lactose-containing whey. This new evidence emphasizes the importance of pottery vessels in processing dairy products, particularly in the manufacture of reduced-lactose milk products among lactose-intolerant prehistoric farming communities6, 7.

Article:
Evidence of world’s ‘oldest’ cheese-making found

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By Team FPS – December 23, 2012

High Heeled Shoes: A Real Pain

Also see:
Shod versus Unshod
Sarah Jessica Parker: Wearing high heels for years mangled my feet
ISU study finds high heels may lead to joint degeneration and knee osteoarthritis

FEBRUARY 2001 PODIATRY MANAGEMENT p. 129-38
Footwear: The Primary Cause of Foot Disorders A continuation of the scientific review of the failings of modern shoes.
By William A. Rossi, D.P.M.

From "Why Shoes Make “Normal” Gait Impossible" by by William A. Rossi, D.P.M.

Why Shoes Make “Normal” Gait Impossible: How flaws in footwear affect this complex human function.
William A. Rossi, D.P.M.

J Exp Biol 213, 2582-2588. August 1, 2010
On muscle, tendon and high heels
R. Csapo, C. N. Maganaris, O. R. Seynnes, and M. V. Narici
Wearing high heels (HH) places the calf muscle–tendon unit (MTU) in a shortened position. As muscles and tendons are highly malleable tissues, chronic use of HH might induce structural and functional changes in the calf MTU. To test this hypothesis, 11 women regularly wearing HH and a control group of 9 women were recruited. Gastrocnemius medialis (GM) fascicle length, pennation angle and physiological cross-sectional area (PCSA), the Achilles’ tendon (AT) length, cross-sectional area (CSA) and mechanical properties, and the plantarflexion torque–angle and torque–velocity relationships were assessed in both groups. Shorter GM fascicle lengths were observed in the HH group (49.6±5.7 mm vs 56.0±7.7 mm), resulting in greater tendon-to-fascicle length ratios. Also, because of greater AT CSA, AT stiffness was higher in the HH group (136.2±26.5 N mm–1 vs 111.3±20.2 N mm–1). However, no differences in the GM PCSA to AT CSA ratio, torque–angle and torque–velocity relationships were found. We conclude that long-term use of high-heeled shoes induces shortening of the GM muscle fascicles and increases AT stiffness, reducing the ankle’s active range of motion. Functionally, these two phenomena seem to counteract each other since no significant differences in static or dynamic torques were observed.

J Appl Biomech. 2012 Feb;28(1):20-8.
Walking on high heels changes muscle activity and the dynamics of human walking significantly.
Simonsen EB, Svendsen MB, Nørreslet A, Baldvinsson HK, Heilskov-Hansen T, Larsen PK, Alkjær T, Henriksen M.
The aim of the study was to investigate the distribution of net joint moments in the lower extremities during walking on high-heeled shoes compared with barefooted walking at identical speed. Fourteen female subjects walked at 4 km/h across three force platforms while they were filmed by five digital video cameras operating at 50 frames/second. Both barefooted walking and walking on high-heeled shoes (heel height: 9 cm) were recorded. Net joint moments were calculated by 3D inverse dynamics. EMG was recorded from eight leg muscles. The knee extensor moment peak in the first half of the stance phase was doubled when walking on high heels. The knee joint angle showed that high-heeled walking caused the subjects to flex the knee joint significantly more in the first half of the stance phase. In the frontal plane a significant increase was observed in the knee joint abductor moment and the hip joint abductor moment. Several EMG parameters increased significantly when walking on high-heels. The results indicate a large increase in bone-on-bone forces in the knee joint directly caused by the increased knee joint extensor moment during high-heeled walking, which may explain the observed higher incidence of osteoarthritis in the knee joint in women as compared with men.

J Am Podiatr Med Assoc. 2003 Jan-Feb;93(1):27-32.
Kinetics of high-heeled gait.
Esenyel M, Walsh K, Walden JG, Gitter A.
A within-subject comparative study of walking while wearing low-heeled sports shoes versus high-heeled dress shoes was performed to identify and describe changes in lower-extremity joint kinetics associated with wearing high-heeled shoes during level overground walking. A volunteer sample of 15 unimpaired female subjects recruited from the local community underwent quantitative measurement of sagittal and frontal plane lower-extremity joint function, including angular motion, muscular moment, power, and work. When walking in high-heeled shoes, a significant reduction in ankle plantar flexor muscle moment, power, and work occurred during the stance phase, whereas increased work was performed by the hip flexor muscles during the transition from stance to swing. In the frontal plane, increased hip and knee varus moments were present. These differences demonstrate that walking in high-heeled shoes alters lower-extremity joint kinetic function. Reduced effectiveness of the ankle plantar flexors during late stance results in a compensatory enhanced hip flexor “pull-off” that assists in limb advancement during the stance-to-swing transition. Larger muscle moments and increased work occur at the hip and knee, which may predispose long-term wearers of high-heeled shoes to musculoskeletal pain.

Ergonomics. 1985 Jul;28(7):965-75.
Falls in the healthy elderly: predisposing causes.
Gabell A, Simons MA, Nayak US.
One hundred healthy men and women aged 65-85 took part in a prospective study. They were clinically examined and underwent laboratory tests of gait, balance and reaction time at the start of an observation year.

All falls occurring in that year were analysed in detail. Three-quarters of them were trips or slips; however, ten personal factors were identified which, if present, increased the likelihood of a fall occurring. These were: disturbance of gait following a rest period accompanied by a lighting change (in persons aged 70 and over); an absent or abnormal plantar reflex; failure to wear prescribed spectacles; the presence of anxiety/depression, of a foot problem, or of two or more self-perceived limitations on mobility; a history of former wearing of high heels; a sustained drop in pulse pressure 5 min after cessation of a rest period; restricted neck movements; and the presence of an inverse Romberg ratio.

The number of circumstantial and personal factors contributing to the falls varied between three and twelve.

 

From "Why Shoes Make “Normal” Gait Impossible" by by William A. Rossi, D.P.M.

 

Lancet. 1998 May 9;351(9113):1399-401.
Knee osteoarthritis and high-heeled shoes.
Kerrigan DC, Todd MK, Riley PO.
BACKGROUND:
Little is known about the effects of walking in high heels on joints in the legs. Since osteoarthritis of the knee is twice as common in women as in men, we investigated torques (forces applied about the leg joints) of women who wore high-heeled shoes.
METHODS:
We studied 20 healthy women who were comfortable wearing high-heeled shoes. The women walked with their own high-heeled shoes and barefoot. Data were plotted and qualitatively compared; major peak values for high-heeled and barefoot walking were statistically compared. Bonferroni adjustment was made for multiple comparisons.
FINDINGS:
Measurement showed increased force across the patellofemoral joint and a greater compressive force on the medial compartment of the knee (average 23% greater forces) during walking in high heels than barefoot.
INTERPRETATION:
The altered forces at the knee caused by walking in high heels may predispose to degenerative changes in the joint.

Gait Posture. 2002 Feb;15(1):56-63.
Analysis of muscular fatigue and foot stability during high-heeled gait.
Gefen A, Megido-Ravid M, Itzchak Y, Arcan M.
Plantar pressure measurements and surface electromyography (EMG) were used to determine the effects of muscular fatigue induced by high-heeled gait. The medio-lateral (M/L) stability of the foot was characterized by measuring the M/L deviations of the center of pressure (COP) and correlating these data with fatigue of lower-limb muscles seen on EMG. EMG measurements from habitual high-heeled shoe wearers demonstrated an imbalance of gastrocnemius lateralis versus gastrocnemius medialis activity in fatigue conditions, which correlated with abnormal lateral shifts in the foot-ground or shoe-ground COP of these women.

Arch Phys Med Rehabil. 2005 May;86(5):871-5.
Moderate-heeled shoes and knee joint torques relevant to the development and progression of knee osteoarthritis.
Kerrigan DC, Johansson JL, Bryant MG, Boxer JA, Della Croce U, Riley PO.
OBJECTIVE:
To determine if women’s dress shoes with heels of just 1.5 in (3.8 cm) in height increases knee joint torques, which are thought to be relevant to the development and/or progression of knee osteoarthritis (OA) in both the medial and patellofemoral compartments.
DESIGN:
Randomized controlled trial.
SETTING:
A 3-dimensional motion analysis gait laboratory.
PARTICIPANTS:
Twenty-nine healthy young women (age, 26.7+/-5.0 y) and 20 healthy elderly adult women (age, 75.3+/-6.5 y).
INTERVENTIONS:
Not applicable.
MAIN OUTCOME MEASURES:
Peak external varus knee torque in early and late stance and prolongation of flexor knee torque in early stance. Three-dimensional data on lower-extremity torques and motion were collected during walking while (1) wearing shoes with 1.5-in high heels and (2) wearing control shoes without any additional heel. Data were plotted and qualitatively compared; major peak values and timing were statistically compared between the 2 conditions using paired t tests.
RESULTS:
Peak knee varus torque during late stance was statistically significantly greater with the heeled shoes than with the controls, with increases of 14% in the young women and 9% in the elderly women. With the heeled shoes, the early stance phase knee flexor torque was significantly prolonged, by 19% in the young women and by 14% in elderly women. Also, the peak flexor torque was 7% higher with the heeled shoe in the elderly women.
CONCLUSIONS:
Even shoes with moderately high heels (1.5 in) significantly increase knee torques thought to be relevant in the development and/or progression of knee OA. Women, particularly those who already have knee OA, should be advised against wearing these types of shoes.

Lancet. 2001 Apr 7;357(9262):1097-8.
Women’s shoes and knee osteoarthritis.
Kerrigan DC, Lelas JL, Karvosky ME.
We assessed whether wearing wide-heeled shoes has a similar effect on knee torque to narrow-heeled shoes by measuring the joint torques of 20 healthy women during walking. Wearing wide-heeled shoes had a 30% greater effect on peak external knee flexor torque than walking barefoot. Walking with wide-heeled and narrow-heeled shoes increased peak knee varus torque by 26% and 22%, respectively. Our findings imply that wide-heeled shoes cause abnormal forces across the patellofemoral and medial compartments of the knee, which are the typical anatomical sites for degenerative joint changes.

J Public Health Med. 2002 Jun;24(2):77-84.
The prevalence of foot problems in older women: a cause for concern.
Dawson J, Thorogood M, Marks SA, Juszczak E, Dodd C, Lavis G, Fitzpatrick R.
BACKGROUND:
Painful feet are an extremely common problem amongst older women. Such problems increase the risk of falls and hamper mobility. The aetiology of painful and deformed feet is poorly understood.
METHODS:
Data were obtained during a pilot case-control study about past high heel usage in women, in relation to osteoarthritis of the knee. A total of 127 women aged 50-70 were interviewed (31 cases, 96 controls); case-control sets were matched for age. The following information was obtained about footwear: (1) age when first wore shoes with heels 1, 2 and 3 inches high; (2) height of heels worn for work; (3) maximum height of heels worn regularly for work, going out socially and for dancing, in 10-year age bands. Information about work-related activities and lifetime occupational history was gathered using a Life-Grid. The interview included a foot inspection.
RESULTS:
Foot problems, particularly foot arthritis, affected considerably more cases than controls (45 per cent versus 16 per cent, p = 0.001) and was considered a confounder. Cases were therefore excluded from subsequent analyses. Amongst controls, the prevalence of any foot problems was very high (83 per cent). All women had regularly worn one inch heels and few (8 per cent) had never worn 2 inch heels. Foot problems were significantly associated with a history of wearing relatively lower heels. Few work activities were related to foot problems; regular lifting was associated with foot pain (p = 0.03).
CONCLUSION:
Most women in this age-group have been exposed to high-heeled shoes over many years, making aetiological research difficult in this area. Foot pain and deformities are widespread. The relationship between footwear, occupational activities and foot problems is a complex one that deserves considerably more research.

Clin Orthop Relat Res. 2000 Mar;(372):69-73.
Anterior knee pain in females.
Fulkerson JP, Arendt EA.
There are clear differences between men and women regarding anterior knee pain. Anatomic factors including increased pelvic width and resulting excessive lateral thrust on the patella are primary factors that predispose females to anterior knee pain. Effects of estrogen on connective tissue synthesis have been reported, but there is no clear mechanism by which this would affect anterior knee pain. Postural and sociologic factors such as wearing high heels and sitting with legs adducted can influence the incidence and severity of anterior knee pain in women.

Am J Phys Med Rehabil. 1991 Oct;70(5):246-54.
Footwear and posture. Compensatory strategies for heel height.
de Lateur BJ, Giaconi RM, Questad K, Ko M, Lehmann JF.
The belief that wearing high-heeled shoes increases lumbar lordosis is firmly ingrained in clinical folklore. Proponents of negative heel footwear argue that because high positive heels increase the lumbar lordosis, negative heels will decrease the lumbar lordosis. Quantitative documentation of the assumption regarding high heels is not to be found in the literature, although sporadic attempts to prove this assumption have been made throughout the 20th Century. Although other effects, such as decreased gait speed and step length, and increased knee flexion at heel strike have been found in more than one study, no increase in lumbar lordosis has been found. Where an actual decrease in lordosis has been found, authors tend to explain it away as inconsistent with what every clinician feels that he or she has observed. We felt it appropriate, then, to conduct both a static and a dynamic study to assess the effects of heel height on lumbar spine and lower limb joint kinematics in the sagittal plane, as well as other strategies to compensate for heel height. The results indicate that the greatest compensation is at the ankle and knee. Where a significant effect occurred in the lumbar spine (males, dynamic study), high heels decreased the lumbar lordosis, i.e., resulted in less swayback rather than more.

J Orthop Sports Phys Ther. 1995 Feb;21(2):94-9.
Effect of positive heel inclination on posture.
Franklin ME, Chenier TC, Brauninger L, Cook H, Harris S.
Millions of women wear high heels on a daily basis; however, few studies have analyzed the changes high heels (positive heel inclination) have on posture. The purpose of this study was to determine whether positive heel inclination changed the postural alignment of the head, spine, pelvis, and knees. Fifteen female college students ((mean age = 22.7, SD = 3.7 years) had sagittal plane angles measured for the cervical spine, thoracic spine, lumbar spine, sacral spine, and knee joints in addition to anterior/posterior displacements of the head and pelvis. All variables were assessed by a Metrecom Skeletal Analysis System, a three-dimensional electrogoniometer. Six randomized trials, three at zero heel inclination and three at 5 cm positive heel inclination, were measured. Analysis of variance results indicated positive heel inclination of subjects brought about significantly lower anterior pelvic tilt, lumbar lordosis, and sacral base angles when compared with zero heel inclination (p < .01). Clinically, patients with low back pain may be affected by high heel usage because of the reduction of the normal lumbar lordosis.

Gerontology. 2005 Sep-Oct;51(5):346-51.
Footwear characteristics and foot problems in older people.
Menz HB, Morris ME.
BACKGROUND:
Foot problems are common in older people, however the contribution of incorrectly fitting footwear and heel elevation to the development of foot pain and deformity has not been fully evaluated.
OBJECTIVES:
To examine the relationship between footwear characteristics and the prevalence of common forefoot problems in older people.
METHODS:
Presence of foot pain and deformity were identified in 176 people (56 men and 120 women) aged 62-96 years (mean 80.09, SD 6.42) using a questionnaire and clinical assessment. Shoe fit was determined by comparing length, width and area measurements of shoes with foot measurements. Past and present use of high heels in women was documented, and heel elevation of footwear was measured.
RESULTS:
Most subjects wore shoes narrower than their feet. Women wore shoes that were shorter, narrower and had a reduced total area compared to their feet than men. Wearing shoes substantially narrower than the foot was associated with corns on the toes, hallux valgus deformity and foot pain, whereas wearing shoes shorter than the foot was associated with lesser toe deformity. Wearing shoes with heel elevation greater than 25 mm was associated with hallux valgus and plantar calluses in women.
CONCLUSION:
Incorrectly fitting footwear is common in older people and is strongly associated with forefoot pathology and foot pain. These findings highlight the need for footwear assessment in the management of foot problems in older people.

J South Orthop Assoc. 1994 Winter;3(4):268-72.
The shod foot and its implications for American women.
Rudicel SA.
Throughout history, members of human societies have gone barefoot, and those societies seemingly had a low incidence of foot deformities and pain. Only one study has addressed the problem of infection through injury to the bare foot; otherwise, the unshod foot seems to have had minimal problems. Initially shoes were made in the shape of the foot and were sandals. Over time, shoes became decorative items and symbols of status and vanity. As the shape of shoes changed, they became deforming forces on the foot and the source of pain. Recent studies by the Council on Women’s Footwear of the American Orthopaedic Foot and Ankle Society have tried to document the problems caused by shoes on the feet of American women. Attempts should continue to educate women on appropriate shoes and proper fit.

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By Team FPS – December 20, 2012

Shod versus Unshod

Also see:
High Heeled Shoes: A Real Pain
The Effects Of Shoes On Foot Strike, Performance
Why Shoes Make “Normal” Gait Impossible
Kit Laughlin – Foot Sequence

Nature. 2010 Jan 28;463(7280):531-5. doi: 10.1038/nature08723.
Foot strike patterns and collision forces in habitually barefoot versus shod runners
Lieberman DE, Venkadesan M, Werbel WA, Daoud AI, D’Andrea S, Davis IS, Mang’eni RO, Pitsiladis Y.
Humans have engaged in endurance running for millions of years, but the modern running shoe was not invented until the 1970s. For most of human evolutionary history, runners were either barefoot or wore minimal footwear such as sandals or moccasins with smaller heels and little cushioning relative to modern running shoes. We wondered how runners coped with the impact caused by the foot colliding with the ground before the invention of the modern shoe. Here we show that habitually barefoot endurance runners often land on the fore-foot (fore-foot strike) before bringing down the heel, but they sometimes land with a flat foot (mid-foot strike) or, less often, on the heel (rear-foot strike). In contrast, habitually shod runners mostly rear-foot strike, facilitated by the elevated and cushioned heel of the modern running shoe. Kinematic and kinetic analyses show that even on hard surfaces, barefoot runners who fore-foot strike generate smaller collision forces than shod rear-foot strikers. This difference results primarily from a more plantarflexed foot at landing and more ankle compliance during impact, decreasing the effective mass of the body that collides with the ground. Fore-foot- and mid-foot-strike gaits were probably more common when humans ran barefoot or in minimal shoes, and may protect the feet and lower limbs from some of the impact-related injuries now experienced by a high percentage of runners.

FEBRUARY 2001 PODIATRY MANAGEMENT p. 129-38
Footwear: The Primary Cause of Foot Disorders A continuation of the scientific review of the failings of modern shoes.
By William A. Rossi, D.P.M.

Why Shoes Make “Normal” Gait Impossible: How flaws in footwear affect this complex human function.
William A. Rossi, D.P.M.

J Biomech. 1995 Jul;28(7):817-27.
Influence of shoes and heel strike on the loading of the hip joint.
Bergmann G, Kniggendorf H, Graichen F, Rohlmann A.
The forces and moments acting at the hip joint influence the long-term stability of the fixation of endoprostheses and the course of coxarthrosis. These loads may depend on the kind of footwear and the walking or running style. These factors were investigated in a patient with instrumented hip implants. He wore different sports shoes, normal leather shoes, hiking boots and clogs and walked barefoot with soft, normal and hard heel strikes. The loads were lowest while walking and jogging without shoes. All shoes increased the joint force and the bending moment at the implant slightly but the torsional moment rose by up to 50%. No relation was found between the different type of shoes and the load increase, only shoes with very hard soles were clearly disadvantageous. Soft heels, soles or insoles did not offer advantages. Gait stability seems to play the most important role in increasing the joint loading and should be the criterion for the choice of footwear. Smooth gait patterns with soft heel strikes are the only means to reduce joint loading during slow jogging.

Footwear Science Volume 1, Issue 2, 2009 pages 81-94
The effects of habitual footwear use: foot shape and function in native barefoot walkers
K. D’Aout, T.C. Pataky, D. De Clercq & P. Aertsad
The human foot was anatomically modern long before footwear was invented, and is adapted to barefoot walking on natural substrates. Understanding the biomechanics of habitually barefoot walkers can provide novel insights both for anthropologist and for applied scientists, yet the necessary data is virtually non-existent. To start assessing morphological and functional effects of the habitual use of footwear, we have studied a population of habitually barefoot walkers from India (n = 70), and compared them with a habitually shod Indian control group (n = 137) and a Western population (n = 48). We focused on foot metrics and on the analysis of plantar pressure data, which was performed using a novel, pixel based method (Pataky and Goulermas 2008, Journal of Biomechanics, 41, 2136). Habitually shod Indians wore less often, and less constricting shoes than Western people. Yet, we found significant differences with their habitually barefoot peers, both in foot shape and in pressure distribution. Barefoot walkers had wider feet and more equally distributed peak pressures, i.e. the entire load carrying surface was contributing more uniformly than in habitually shod subjects, where regions of very high or very low peak pressures were more apparent. Western subjects differed strongly from both Indian populations (and most from barefoot Indians), by having relatively short and, especially, slender feet, with more focal and higher peak pressures at the heel, metatarsals and hallux. The evolutionary history of humans shows that barefoot walking is the biologically natural situation. The use of footwear remains necessary, especially on unnatural substrates, in athletics, and in some pathologies, but current data suggests that footwear that fails to respect natural foot shape and function will ultimately alter the morphology and the biomechanical behaviour of the foot.

J Biomech. 2000 Mar;33(3):269-78.
Biomechanical analysis of the stance phase during barefoot and shod running.
De Wit B, De Clercq D, Aerts P.
This study investigated spatio-temporal variables, ground reaction forces and sagittal and frontal plane kinematics during the stance phase of nine trained subjects running barefoot and shod at three different velocities (3.5, 4.5, 5.5 m s(-1)). Differences between conditions were detected with the general linear method (factorial model). Barefoot running is characterized by a significantly larger external loading rate than the shod condition. The flatter foot placement at touchdown is prepared in free flight, implying an actively induced adaptation strategy. In the barefoot condition, plantar pressure measurements reveal a flatter foot placement to correlate with lower peak heel pressures. Therefore, it is assumed that runners adopt this different touchdown geometry in barefoot running in an attempt to limit the local pressure underneath the heel. A significantly higher leg stiffness during the stance phase was found for the barefoot condition. The sagittal kinematic adaptations between conditions were found in the same way for all subjects and at the three running velocities. However, large individual variations were observed between the runners for the rearfoot kinematics.

Bone Joint Surg Br. 1992 Jul;74(4):525-7.
The influence of footwear on the prevalence of flat foot. A survey of 2300 children.
Rao UB, Joseph B.
We analysed static footprints of 2300 children between the ages of four and 13 years to establish the influence of footwear on the prevalence of flat foot. The incidence among children who used footwear was 8.6% compared with 2.8% in those who did not (p less than 0.001). Significant differences between the predominance in shod and unshod children were noted in all age groups, most marked in those with generalised ligament laxity. Flat foot was most common in children who wore closed-toe shoes, less common in those who wore sandals or slippers, and least in the unshod. Our findings suggest that shoe-wearing in early childhood is detrimental to the development of a normal longitudinal arch.

Med Sci Sports Exerc. 1987 Apr;19(2):148-56.
Running-related injury prevention through barefoot adaptations.
Robbins SE, Hanna AM.
A number of reports indicate an extremely low running-related injury frequency in barefoot populations in contrast to reports about shod populations. It is hypothesized that the adaptations which produce shock absorption, an inherent consequence of barefoot activity and a mechanism responsible for the low injury frequency in unshod populations, are related to deflection of the medial longitudinal arch of the foot on loading. It is also hypothesized that the known inability of this arch of the shod foot to deflect without failure (foot rigidity) is responsible for the high injury frequency in shod populations. To evaluate these hypotheses, 17 recreational runners were analyzed to study the adaptive pattern of the medial longitudinal arch of the foot due to increased barefoot weight-bearing activity. Changes occurred in the medial longitudinal arch which allowed deflection of this arch on loading which substantiated the hypotheses. Other evidence suggests that sensory feedback largely from the glabrous epithelium of the foot is the element of barefoot activity which induced these adaptations. The sensory insulation inherent in the modern running shoe appears responsible for the high injury frequency associated with running. The injuries are considered “pseudo-neuropathic” in nature.

Med Sci Sports Exerc. 1989 Apr;21(2):130-9.
Running-related injury prevention through innate impact-moderating behavior.
Robbins SE, Gouw GJ, Hanna AM.
The purpose of these experiments was to test the Robbins and Hanna hypothesis, which relates differences in discomfort from localized deformation at certain positions on the plantar surface to protective behavior (intrinsic foot shock absorption). A penetrometer was used to quantify the relations between localized load and pain and between load and depth of deformation. The magnitude of load required to elicit pain varied significantly (P less than 0.005) in relation to position on the plantar surface. With a load of 9 kg and a 10 mm spherical end on the penetrometer, 6% of the sample reported pain at the heelpad, 32% at the distal first digit, and 66% at the first metatarsal-phalangeal joint. This pattern was predicted by the Robbins and Hanna thesis. Two deformation patterns were observed which were best explained by deformation constraint by tight trabecular tethering of the epithelial membrane at the heelpad and distal first digit and unrestricted deformation due to loose trabecular tethering of the epithelial membrane at the first metatarsal-phalangeal joint. These data provide insight into how, when barefoot, the plantar surface resists perforation yet provides protection to local bony structures. These data further support the notion that plantar sensory feedback plays a central role in safe and effective locomotion.

J Sports Med Phys Fitness. 2009 Mar;49(1):6-13.
Biomechanical and physiological comparison of barefoot and two shod conditions in experienced barefoot runners.
Squadrone R, Gallozzi C.
AIM:
The first aim of this study was to assess how changes in the mechanical characteristics of the foot/shoe-ground interface affect spatio-temporal variables, ground pressure distribution, sagittal plane kinematics, and running economy in 8 experienced barefoot runners. The second aim was to assess if a special lightweight shoe (Vibram Fivefingers) was effective in mimic the experience of barefoot running.
METHODS:
By using an instrumented treadmill, barefoot running, running with the Fivefingers, and running with standard running shoe were compared, analyzing a large numbers of consecutive steps. Foot/shoe-ground interface pressure distribution, lower limb kinematics, V.O(2) and heart rate data were simultaneously collected.
RESULTS:
Compared to the standard shod condition when running barefoot the athletes landed in more plantarflexion at the ankle. This caused reduced impact forces and changes in stride kinematics. In particular, significantly shorter stride length and contact times and higher stride frequency were observed (P<0.05). Compared to standard shod condition, V.O(2) and peak impact forces were significantly lower with Fivefingers (P<0.05) and much closer to barefoot running. Lower limb kinematics with Fivefingers was similar to barefoot running with a foot position which was significantly more plantarflexed than in control shoe (P<0.05).
CONCLUSIONS:
The data of this study support the assumption that changes in the foot-ground interface led to changes in running pattern in a group of experienced barefoot runners. The Fivefingers model seems to be effective in imitating the barefoot conditions while providing a small amount of protection.

J Biomech. 2003 Aug;36(8):1169-76.
Changes in EMG signals for the muscle tibialis anterior while running barefoot or with shoes resolved by non-linearly scaled wavelets.
von Tscharner V, Goepfert B, Nigg BM.
The purpose of this project was to study the EMG pattern of the tibialis anterior muscle in heel-toe running. Specifically, EMG changes in time, intensity and frequency shortly before and after heel-strike were addressed using an EMG-specific non-linearly scaled wavelets analysis. This method allowed extracting the time, intensity and frequency information inherent in the EMG signal at any time. The EMG signals of 40 male subjects were recorded for running barefoot and with shoes. The results confirmed that the pre-heel-strike EMG activities were typically seen at higher EMG frequencies (60-270Hz) while the post-heel-strike EMG activities resulted in lower frequency signals (10-90Hz). The timing of the pre-heel-strike EMG activities was not influenced by the used shoe conditions. The timing of the post-heel-strike EMG activities was significantly delayed when wearing shoes. The intensity of the pre-heel-strike muscle activity increased compared to the post-heel-strike one when wearing shoes. One can conclude that the activity of the tibialis anterior adjusts specifically to exterior conditions. The frequency shift between pre- and post heel-strike muscle activity were discussed with respect to activation of different motor units.

Curr Sports Med Rep. 2009 Sep-Oct;8(5):262-6. doi: 10.1249/JSR.0b013e3181b9e3be.
Foot and ankle injuries in the barefoot sports.
Vormittag K, Calonje R, Briner WW.
Playing sports barefoot has been contested since the very beginnings of athletic competition. Even today, some data suggest that shoes may limit the adaptive pronation that occurs after footstrike during running gait. This pronation likely protects runners from injury. Boardsport participants who perform their sports barefoot on the water seem to be at risk for foot and ankle injuries. The high-impact forces in gymnastics place participants at risk for foot and ankle injuries, as well. Swimming and diving have a low rate of foot and ankle injuries. The risk of ankle sprain in beach volleyball, which is played barefoot, seems to be lower than that for indoor volleyball, played wearing shoes. Martial arts place competitors at risk for injuries to the foot and ankle from torsional and impact mechanisms. Athletes who hope to return to barefoot competition after injury should perform their rehabilitation in their bare feet.

Med Sci Sports Exerc. 2007 Feb;39(2):330-9.
Gait-related risk factors for exercise-related lower-leg pain during shod running.
Willems TM, Witvrouw E, De Cock A, De Clercq D.
PURPOSE:
Exercise-related lower-leg pain (ERLLP) is a common chronic sports injury. In clinical practice, deviant gait biomechanics are frequently considered to play a role in the development of ERLLP, although there is scarce scientific evidence that gait-related variables predispose athletes to this injury. The purpose of this study was to examine prospectively the gait-related risk factors for ERLLP during shod running in a young, physically active population.
METHODS:
The gait pattern during shod running of 400 physical education students was evaluated at the beginning of their academic study. This was accomplished by means of plantar pressure measurements and 3D gait kinematics. After this evaluation, the same sports physician registered all sports injuries during this study.
RESULTS:
During the follow-up period, 46 subjects developed ERLLP, of whom 29 subjects had bilateral complaints. Thus, 75 symptomatic lower legs (35 left and 40 right) were classified into the ERLLP group. Bilateral feet of 167 subjects who sustained no injuries at the lower extremities served as the referent group. Cox regression analysis revealed that subjects who will develop ERLLP have an altered running pattern compared with the referent subjects. More specifically, these subjects showed a significantly increased pronation excursion, accompanied by more pressure underneath the medial side of the foot, a delayed maximal eversion, and an accelerated reinversion.
CONCLUSION:
The findings of this study suggest that altered gait biomechanics during shod running play a role in the genesis of ERLLP and, thus, should be considered in prevention and rehabilitation of this pathology.

The Foot Volume 17, Issue 4 , Pages 205-213, December 2007
Shod versus unshod: The emergence of forefoot pathology in modern humans?
B. Zipfel, L.R. Berger
Background
Pathologies of the metatarsal bones in contemporary humans are common yet it remains unclear from an evolutionary perspective to what extent, if any, footwear and other environmental factors such as modern substrates have contributed to the emergence of common metatarsal pathological changes.
Objectives
To investigate the frequency of metatarsal bone pathologies in contemporary and habitually unshod pre-historic people in order to ascertain whether these frequencies are affected by variation in habitual behaviour, the wearing of footwear and/or exposure to modern substrates.
Method
The metatarsal elements from four human groups were examined for pathological variation. Three of these skeletal samples were from recent rural and urban shod populations (Sotho, Zulu and European) and one from habitually unshod pre-pastoral Holocene people who practiced a subsistence hunter gatherer lifestyle.
Results
The trends in the dominance of pathological lesions between the five metatarsal bones were broadly similar in all four samples. In all groups the first metatarsal presented with the greatest number of pathological lesions; more specifically, at the first metatarsal head. The Sotho and European groups presented with notably greater frequencies of pathological changes followed by the Zulu group and then the pre-pastoral.
Conclusions
The pathological lesions found in the metatarsals of the three recent human groups generally appeared to be more severe than those found in the pre-pastoral group. This result may support the hypothesis that pathological variation in the metatarsus was affected by habitual behaviour including the wearing of footwear and exposure to modern substrates.

Clin J Sport Med. 2001 Jan;11(1):2-9.
The role of impact forces and foot pronation: a new paradigm.
Nigg BM.
OBJECTIVE:
This article discusses the possible association between impact forces and foot pronation and the development of running-related injuries, and proposes a new paradigm for impact forces and foot pronation.
DATA SOURCES:
The article is based on a critical analysis of the literature on heel-toe running addressing kinematics, kinetics, resultant joint movements and forces, muscle activity, subject and material characteristics, epidemiology, and biologic reactions. However, this paper is not a review of the literature but rather an attempt to replace the established concepts of impact forces and movement control with a new paradigm that would allow explaining some of the current contradictions in this topic of research.
STUDY SELECTION:
The analysis included all papers published on this topic over the last 25 years. For the last few years, it concentrated on papers expressing critical concerns on the established concepts of impact and movement control.
DATA EXTRACTION:
An attempt was made to find indications in the various publications to support or reject the current concept of impact forces and movement control. Furthermore, the results of the available studies were searched for indications expanding the current understanding of impact forces and movement control in running.
DATA SYNTHESIS:
Data were synthesized revealing contradictions in the experimental results and the established concepts. Based on the contradictions in the existing research publications, a new paradigm was proposed.
CONCLUSION:
Theoretical, experimental, and epidemiological evidence on impact forces showed that one cannot conclude that impact forces are important factors in the development of chronic and/or acute running-related injuries. A new paradigm for impact forces during running proposes that impact forces are input signals that produce muscle tuning shortly before the next contact with the ground to minimize soft tissue vibration and/or reduce joint and tendon loading. Muscle tuning might affect fatigue, comfort, work, and performance. Experimental evidence suggests that the concept of “aligning the skeleton” with shoes, inserts, and orthotics should be reconsidered. They produce only small, not systematic. and subject-specific changes of foot and leg movement. A new paradigm for movement control for the lower extremities proposes that forces acting on the foot during the stance phase act as an input signal producing a muscle reaction. The cost function used in this adaptation process is to maintain a preferred joint movement path for a given movement task. If an intervention counteracts the preferred movement path, muscle activity must be increased. An optimal shoe, insert, or orthotic reduces muscle activity. Thus, shoes, inserts, and orthotics affect general muscle activity and, therefore, fatigue, comfort, work, and performance. The two proposed paradigms suggest that the locomotor system use a similar strategy for “impact” and “movement control.” In both cases the locomotor system keeps the general kinematic and kinetic situations similar for a given task. The proposed muscle tuning reaction to impact loading affects the muscle activation before ground contact. The proposed muscle adaptation to provide a constant joint movement pattern affects the muscle activation during ground contact. However, further experimental and theoretical studies are needed to support or reject the proposed paradigms.

J South Orthop Assoc. 1994 Winter;3(4):268-72.
The shod foot and its implications for American women.
Rudicel SA.
Throughout history, members of human societies have gone barefoot, and those societies seemingly had a low incidence of foot deformities and pain. Only one study has addressed the problem of infection through injury to the bare foot; otherwise, the unshod foot seems to have had minimal problems. Initially shoes were made in the shape of the foot and were sandals. Over time, shoes became decorative items and symbols of status and vanity. As the shape of shoes changed, they became deforming forces on the foot and the source of pain. Recent studies by the Council on Women’s Footwear of the American Orthopaedic Foot and Ankle Society have tried to document the problems caused by shoes on the feet of American women. Attempts should continue to educate women on appropriate shoes and proper fit.

J Strength Cond Res. 2013 Mar;27(3):733-7. doi: 10.1519/JSC.0b013e318280c9ce.
Effects of different footwear on vertical jump and landing parameters.
Laporta JW, Brown LE, Coburn JW, Galpin AJ, Tufano JJ, Cazas VL, Tan JG.
Little is known about the effects of different footwear on anaerobic performance variables. The purpose of this study was to investigate the effect of different footwear on vertical jumping and landing parameters. Ten men and 10 women participated. After a dynamic warm-up, subjects performed a vertical jump (VJ), depth drop (DD), and Bosco test on a force plate in 3 different conditions, on 3 separate days: bare feet (BF), minimalist footwear (MF), and tennis shoes (TS). Bare feet had greater relative peak power (relPP) in the VJ (men: BF, 59.87 ± 5.09 W⋅kg; MF, 58.39 ± 5.69 W·kg; TS, 57.70 ± 6.54 W·kg; women: BF, 45.26 ± 4.10 W·kg; MF, 45.06 ± 3.53 W·kg; TS, 44.77 ± 4.55 W·kg), while for men, jump height (JH) was also greater in BF and MF (BF, 44.5 ± 4.46 cm; MF, 43.47 ± 5.5 cm; TS, 41.47 ± 14.45 cm). Results of the Bosco test revealed average relPP was greatest in BF compared with MF and TS (men: BF, 19.70 ± 3.01 W·kg; MF, 19.28 ± 3.00 W·kg; TS, 18.93 ± 3.33 W·kg; women: BF, 14.68 ± 1.41 W·kg; MF, 13.97 ± 1.56 W·kg; TS 13.62 ± 1.67 W·kg), while for JH, BF and MF were greater than TS (men: BF, 28.62 ± 5.0 cm; MF, 27.78 ± 5.09 cm; TS, 26.54 ± 5.1 cm; women: BF, 18.60 ± 1.97 cm; MF, 17.86 ± 6.35 cm; TS, 17.35 ± 2.47 cm). No differences in relative impact force were seen during the DD between conditions. Therefore, athletes and coaches interested in enhancing single and multiple VJs might consider either BF or minimalist shoes.

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By Team FPS – December 20, 2012

Heart Arrhythmia

Also see:
Protect the Mitochondria
Thyroid Status and Cardiovascular Disease
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
The Cholesterol and Thyroid Connection
High Blood Pressure and Hypothyroidism
A Cure for Heart Disease
Hypothyroidism and A Shift in Death Patterns
High Estrogen and Heart Disease in Men
Unsaturated Fats and Heart Damage
Estrogen Dominance and Magnesium Deficiency
Aldosterone as an endogenous cardiovascular toxin
Aldosterone and Thrombosis
Sodium Deficiency and Stress
Low Sodium Diet: High FFA, Insulin Resistance, Atherosclerosis
Sodium and Mortality: An Inverse Relationship
Ray Peat, PhD Quotes on Coconut Oil
Thyroid Hormones: The Ultimate Weapon Against Heart Disease?

All italic quotes by Ray Peat, PhD.

“Progesterone increases the heart’s pumping efficiency, and estrogen is antagonistic, and can produce cardiac arrhythmia.”

“Progesterone, which helps to maintain blood volume (partly by preventing vascular leakiness, preventing excessive sodium loss and by supporting albumin synthesis) antagonizes aldosterone. Aldosterone antagonists are now being recognized as effective treatments for hypertension, water retention, congestive heart failure, arrhythmia, diabetes, kidney disease, and a great variety of inflammatory problems.”

“Vitamins D and K, and calcium are important for stabilizing the heart rhythm. Estrogen tends to cause chemical hyperventilation (loss of carbon dioxide), which increases blood viscosity and the tendency toward atrial fibrillation. Progesterone and those other steroids have opposite effects (progesterone is a natural aldosterone antagonist, too). Thyroid is essential for helping cells to retain magnesium. A quart or two of milk, and a glass or two of orange juice every day helps with the main stabilizing minerals, but it’s good to have sea food once a week, especially shell fish, for the trace minerals.”

“A complete list of protective nutritional chemicals and natural drugs or analogs to our endogenous protective factors would be very long, but we should give special thought to certain ones, including succinic acid, which stimulates respiration and protective steroid synthesis; thyroid and vitamin E, which promote normal oxidation while preventing abnormal oxidation; magnesium; sodium and lithium, which help us to retain magnesium; tropical fruits, which contain GHB; coconut oil, which protects against cardiac necrosis, lipid peroxidation, hypothyroidism, hypoglycemia, and histamine damage; valium agonists, natural antihistamines; adenosine and uridine. Visits to higher elevations, and exposure’ to bright, long-wave light, can cause the body to optimize its own anti-stress chemistry. Avoiding the sense of being trapped is a high-level adaptive factor.”

Low DHEA:
“Albert Szent-Györgyi showed that the heart responds to progesterone, and more recently other researchers have presented evidence that DHEA is our “endogenous digitalis.”

Eur J Prev Cardiol. 2012 Nov 14. [Epub ahead of print]
Dehydroepiandrosterone sulfate levels and risk of atrial fibrillation: The Rotterdam Study.
Krijthe BP, de Jong FH, Hofman A, Franco OH, Witteman JC, Stricker BH, Heeringa J.
Background: High plasma dehydroepiandrosterone sulfate (DHEAS) levels have been associated with a reduced risk of cardiovascular disease and atherosclerosis. To our knowledge, no previous follow-up study has investigated the association between DHEAS and the development of atrial fibrillation. Our objective was to investigate the association between DHEAS levels and incident atrial fibrillation.Methods and results: The study was based on a random sample within the prospective population-based Rotterdam Study. The study population comprised 1180 participants without atrial fibrillation at baseline for whom baseline levels of DHEAS were measured in plasma. Atrial fibrillation was ascertained from centre visit electrocardiogram (ECG) assessments as well as medical records. During a mean follow-up period of 12.3 years, 129 participants developed atrial fibrillation. DHEAS levels were inversely associated with the risk of atrial fibrillation (hazard ratio (HR) per standard deviation (SD): 0.74, 95% confidence interval (CI): 0.58-0.94). Subjects in the highest DHEAS quartile had an almost three times lower risk of atrial fibrillation during follow-up, compared to those in the lowest DHEAS quartile (HR: 0.34, 95% CI: 0.18-0.64) adjusted for age, sex and cardiovascular risk factors.Conclusion: DHEAS can be regarded as an important indicator of future atrial fibrillation in both men and women, independent of known cardiovascular risk factors.

Exp Gerontol. 2002 May;37(5):701-12.
Dehydroepiandrosterone-sulfate serum levels and common age-related diseases: results from a cross-sectional Italian study of a general elderly population.
Ravaglia G, Forti P, Maioli F, Sacchetti L, Nativio V, Scali CR, Mariani E,
Zanardi V, Stefanini A, Macini PL.
The association of low serum dehydroepiandrosterone sulfate (DHEAS) levels with age, lifestyle, general health status indicators, and specific diseases was investigated in 436 men and 544 women of 65-97 yr old. In both sexes low serum DHEAS levels were associated with age, alcohol intake, number of current medications, and decreased thyroid function. Low DHEAS was also associated with low serum albumin in men and low systolic blood pressure in women. Compared to healthy men (n=106) age-adjusted serum DHEAS levels were significantly lower in men with atrial fibrillation, chronic obstructive lung disease, dementia, parkinsonism, cancer, diabetes, hypothyroidism, and in institutionalized men. Compared to healthy women (n=100) age-adjusted serum DHEAS levels were significantly lower in women with occlusive arterial disease, chronic obstructive lung disease, and osteoporosis. After controlling for differences in lifestyle and general health status parameters, low DHEAS levels remained statistically associated only with atrial fibrillation in men and osteoporosis in women, and it cannot be excluded that these association were spurious, due to multiple comparisons. These data suggest that in elderly people low serum DHEAS levels are more a non-specific indicator of aging and health status than a risk indicator of specific diseases.

=================================
“Pregnenolone, progesterone, DHEA, testosterone, and thyroid all improve the stability of the heart.”

Reduced testosterone:
J Cardiovasc Electrophysiol. 2009 Sep;20(9):1055-60.
Deficiency of testosterone associates with the substrate of atrial fibrillation in the rat model.
Tsuneda T, Yamashita T, Kato T, Sekiguchi A, Sagara K, Sawada H, Aizawa T, Fu LT, Fujiki A, Inoue H.
BACKGROUND:
Since the prevalence of atrial fibrillation (AF) increases progressively with aging, especially in men, we hypothesized that testosterone might affect the occurrence of AF.
METHODS AND RESULTS:
We examined the electrophysiological properties of the atria in isolated-perfused hearts of sham-operated male (SM), female (SF), orchiectomized male with and without administration of testosterone (ORCH-T and ORCH), and ovariectomized female (OVX) Sprague-Dawley rats. An electrophysiological study revealed that repetitive atrial responses induced by electrical stimuli significantly increased in ORCH rats without changes in other electrophysiological properties and were abolished by administration of testosterone. To investigate the underlying mechanisms, we evaluated the expression level of calcium-handling proteins. In ORCH rats, the immunoreactive protein level of ryanodine receptor type 2 (RyR2) and sodium-calcium exchanger significantly increased as compared with SM and ORCH-T rats without alterations in the level of FK506-binding protein (FKBP12.6), sarcoendoplasmic reticulum Ca-ATPase, and phospholamban. Immunoprecipitation analysis demonstrated decreased binding of FKBP12.6 to RyR2 in ORCH rats, which was prevented by testosterone. In contrast, the expression levels of these proteins showed no significant differences between SF and OVX rats.
CONCLUSION:
Deficiency of testosterone was arrhythmogenic in rat atria possibly through less binding of FKBP12.6 to RyR2, which could induce feasible calcium leakage from the sarcoendoplasmic reticulum. These results would explain, at least in part, the increase in the prevalence of AF in accordance with the decline of testosterone particularly in elderly men.

Clin Cardiol. 2009 Jan;32(1):43-6.
Reduced testosterone levels in males with lone atrial fibrillation.
Lai J, Zhou D, Xia S, Shang Y, Want L, Zheng L, Zhu J.
BACKGROUND:
Sex hormones play an important role in the development of cardiovascular disease. Testosterone and estradiol have been reported to be down-regulated in subjects with coronary artery disease and heart failure, but has not been studied in atrial fibrillation (AF).
HYPOTHESIS:
Levels of sex hormones may be associated with susceptibility to lone AF in men.
METHODS:
Fifty-eight male subjects who had electrocardiographic evidence of paroxysmal or chronic AF and a structurally normal heart on echocardiography were enrolled. Subjects were excluded if they had been taking angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or statins within 3 mo or had a history of coronary artery disease, rheumatic heart disease, cardiomyopathy, significant valvular disease, hyperthyroidism, or hypertension. Fifty-eight controls were recruited from a healthy outpatient population. Serum total testosterone and estradiol levels were determined using a commercially available radioimmunoassay.
RESULTS:
Mean levels of testosterone were significantly lower in subjects with lone AF when compared with controls (476 ng/dl versus 514 ng/dl, p = 0.005). No significant differences were found in the estradiol levels between the 2 groups (31.9 pg/ml versus 32.4 pg/ml, p = 0.789).
CONCLUSION:
Reduced testosterone levels may be associated with susceptibility to lone AF in men.

Med Hypotheses. 2010 Aug;75(2):269-70.
Testosterone as an atrial fibrillation treatment and stroke preventative in aging
men: case histories and hypothesis.
Eby G.

=================================
Hypothyroidism:

“Broda Barnes showed that hypothyroidism causes heart disease, and also causes a tendency toward hypoglycemia. Low thyroid people compensate for the deficiency of energy and glucose (and of oxygen, for reasons similar to those mentioned above) by secreting an excess of adrenalin. Their 24 hour urine metabolites of adrenalin sometimes are 30 or 40 times normal. Recent studies that show that a moderate dose of thyroxin lowers lipid peroxidation confirm that thyroid has an antistress effect. The “conduction block” which occurs in hypothyroidism seems to be the same as the conduction block which develops in stress and predisposes to fibrillation.”

Neth Heart J. 2008 Feb;16(2):57-9.
Hypothyroidism as the cause of atrioventricular block in an elderly patient.
Schoenmakers N, de Graaff WE, Peters RH.
Department of Cardiology, Department of Internal Medicine, Tergooi Hospital
Blaricum, the Netherlands.
Syncope is a common problem in the older patient. Sometimes syncope is caused by
extreme bradycardia secondary to atrioventricular (AV) block. We describe a case
in which a 90-year-old woman presented with complete AV block due to severe
hypothyroidism. After suppletion with levothyroxine, AV conduction was restored.
(Neth Heart J 2008;16:57-9.).

Am J Med. 1990 Jun;88(6):638-41.
Recognition and management of cardiovascular disease related to thyroid dysfunction.
Ladenson PW.
Hypothyroidism and hyperthyroidism are both associated with clinically significant cardiovascular derangements. In hypothyroidism, these include pericardial effusion, heart failure, and the complex interrelationship between hypothyroidism and ischemic heart disease. Cardiovascular disorders associated with hyperthyroidism include atrial tachyarrhythmias, mitral valve dysfunction, and heart failure. Although these usually occur in individuals with intrinsic heart disease, thyroid dysfunction alone rarely causes serious but reversible cardiovascular dysfunction. Patients with commonly encountered cardiac disorders, e.g., idiopathic cardiomyopathy and atrial fibrillation, should be screened for potentially contributing subclinical thyroid diseases. In patients with heart failure and hypothyroidism, initial management should focus on diagnosis and optimal management of any primary cardiac disease, whereas in hyperthyroidism, aggressive measures to control excess thyroid hormone action should generally have the highest priority.

Recent Prog Horm Res. 2004;59:31-50.
Effects of thyroid hormone on the cardiovascular system.
Fazio S, Palmieri EA, Lombardi G, Biondi B.
Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias – namely, atrial fibrillation – whereas overt hypothyroidism is characterized by the opposite changes. However, whether changes in cardiac performance associated with overt thyroid dysfunction are due mainly to alterations of myocardial contractility or to loading conditions remains unclear. Extensive evidence indicates that the cardiovascular system responds to the minimal but persistent changes in circulating thyroid hormone levels, which are typical of individuals with subclinical thyroid dysfunction. Subclinical hyperthyroidism is associated with increased heart rate, atrial arrhythmias, increased LV mass, impaired ventricular relaxation, reduced exercise performance, and increased risk of cardiovascular mortality. Subclinical hypothyroidism is associated with impaired LV diastolic function and subtle systolic dysfunction and an enhanced risk for atherosclerosis and myocardial infarction. Because all cardiovascular abnormalities are reversed by restoration of euthyroidism (“subclinical hypothyroidism”) or blunted by beta-blockade and L-thyroxine (L-T4) dose tailoring (“subclinical hyperthyroidism”), timely treatment is advisable in an attempt to avoid adverse cardiovascular effects. Interestingly, some data indicate that patients with acute and chronic cardiovascular disorders and those undergoing cardiac surgery may have altered peripheral thyroid hormone metabolism that, in turn, may contribute to altered cardiac function. Preliminary clinical investigations suggest that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease.

Pol Arch Med Wewn. 1983 Sep;70(3):81-5.
[Functional disorders of the heart conduction system as a symptom of thyroid hormone deficiency].
[Article in Polish]
Jonderko G, Kocot E, Marcisz C.

Nouv Presse Med. 1975 Jun 21;4(25):1859-62.
[Disorders of intra-cardiac conduction and hypothyroidism in adults. A systematic
study of 42 cases].
[Article in French]
Lardoux H, Cénac A, Perlemuter L, Bernheim R, Hazard J.
The rate of occurrence of disturbances of intracardiac conduction in association with adult hypothyroidism is not well known. On the basis of routine study of the electrocardiograms of 42 non-treated patients, disturbances of conduction were found in almost one third. Left anterior hemiblock (6/42) and first degree atrioventricular block (5/42) are the commonest. Bifascicular involvement is rare. Neither a trifascicular lesion nor complete AV dissociation were seen. There was no evident effect of hormone therapy on conduction disturbances. Their prognosis is good but they should perhaps be taken into consideration when the indications for beta-blockers are weighed.

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Magnesium retention compromised in hypothyroidism.

“Simply eating an adequate amount of calcium and magnesium can alleviate many problems related to stress and aging that are considered serious, such as heart arrhythmia, pancreatitis, and tissue calcification.”

“In hypothyroidism, the brain exciting hormones adrenaline, estrogen, and cortisol are usually elevated, and the nerve-muscle relaxant magnesium is low.”

“Low-thyroid cells are unable to retain magnesium efficiently, and a magnesium deficiency prevents muscle relaxation, wasting energy. Adequate sodium prevents urinary magnesium loss.”

“Magnesium, retained in the cell largely under the influence of ATP and thyroid, is our basic “calcium blocker,” or calcium antagonist.”

“Magnesium, which is protective against excitatory damage and is a calcium antagonist, tends to be retained in proportion to the activity of thyroid hormone.”

Am J Vet Res. 1978 Jan;39(1):159-61.
Effect of thyroid state on magnesium concentration of rat tissues.
Oliver JW.
The effect of alteration of thyroid status by thiouracil (0.1% concentration in drinking water for 60 days) or exogenous thyroxine (25 mg/dg of body weight administered SC from days 30 to 60) on magnesium content of rat tissues following exogenous magnesium was evaluated. Treatment of rats with magnesium solution (25 mg of magnesium sulfate/dg of body weight) resulted in increased magnesium concentration in most tissues of hypothyroid and hyperthyroid rats, with the mesenchymal-derived tissues (aorta, trachea, and ear cartilage) exhibiting the greatest increases (respectively, 154, 130, and 133% of control group values for hypothyroid rats, and 115, 108, and 107% of control group values for the hyperthyroid group). Magnesium concentration in skeletal and cardiac muscle was similar for hyperthyroid and control rats, but magnesium concentration in these same tissues of hypothyroid rats was decreased. Magnesium distribution and retention in rat tissues is altered considerably, depending on the functional status of thyroid gland.

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Consequences of magnesium deficiency on the heart.

Int J Biochem Cell Biol. 1997 Nov;29(11):1273-8.
Magnesium deficiency enhances oxidative stress and collagen synthesis in vivo in the aorta of rats.
Shivakumar K, Kumar BP.
Magnesium deficiency has been shown to produce vascular lesions in experimental animals, but the underlying mechanisms of vascular injury are not clear. It has been reported that in rodents, magnesium deficiency enhances circulating levels of factors that promote free radical generation and are mitogenic. In pursuance of these observations, the present study tested the hypothesis that magnesium deficiency may enhance oxidative stress and trigger an accelerated growth response in vivo in the aorta of rats. Oxidative stress was evaluated in terms of levels of thiobarbituric acid-reactive substances in the serum and aorta and activity of superoxide dismutase and catalase in the aorta; fractional rates of collagen synthesis were assessed using [3H]-proline. Serum and tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. The present study demonstrated for the first time that magnesium deficiency significantly (P < 0.001) increases levels of thiobarbituric acid-reactive substances in the aorta of rats. Other changes in the aorta of animals on the Mg-deficient diet included a significant reduction (54%, P < 0.001) in the activity of superoxide dismutase and catalase (37%, P < 0.01) and a 19% increase in net fractional rates of collagen synthesis (P < 0.05). While serum magnesium was significantly reduced in these animals (P < 0.001), aortic tissue levels of magnesium in these animals remained unaltered throughout the duration of the study, suggesting the existence of other control mechanisms, apart from reduced tissue levels of magnesium, mediating the observed effects. These findings suggest that magnesium deficiency may trigger a wound healing response, involving oxidative injury and growth stimulation, in the vascular system.

Int J Biochem Cell Biol. 1997 Jan;29(1):129-34.
Magnesium deficiency-related changes in lipid peroxidation and collagen metabolism in vivo in rat heart.
Kumar BP, Shivakumar K, Kartha CC.
Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis. As part of the ongoing investigations in this laboratory to establish the biochemical correlates of these histological changes, the present study probed the extent of lipid peroxidation and alterations in collagen metabolism in the heart in rats fed a magnesium-deficient diet for 28, 60 or 80 days. While lipid peroxidation was measured by the thiobarbituric acid reaction, collagen turnover rates and fibroblast proliferation were assessed using [3H]-proline and [3H]-thymidine, respectively. Tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. A 39% increase in the cardiac tissue level of thiobarbituric acid reactive substances was observed on day 60 of deficiency (p < 0.001). A marked drop in collagen deposition rate (59%, p < 0.001%) on day 28 but a significant rise in fractional synthesis rate (12%, p < 0.001) and collagen deposition rate (24%, p < 0.001) on day 60 were observed. A fibroproliferative response in the heart was evident on day 80 but not at earlier time-points. Thus, the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of magnesium. These changes were, however, not directly related to alterations in the tissue levels of Mg. It is suggested that the increase in cardiac collagen synthesis and fibroplasia associated with Mg deficiency may represent reparative fibrogenesis, upon oxidative damage to the cardiac muscle, and is mediated by a mechanism independent of changes in cardiac tissue levels of Mg.

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Serotonin and heart arrhythmia:

Res Commun Chem Pathol Pharmacol. 1990 Jun;68(3):383-6.
5-Hydroxytryptamine (serotonin) enhances ventricular arrhythmias induced by acute
coronary artery ligation in rats.
el-Mahdy SA.
Ventricular arrhythmias were induced by acute coronary artery ligation in anesthetized rats. 5-Hydroxytryptamine (5-HT) in doses of 100-200 micrograms kg-1, given i.v. 5 minutes before coronary artery ligation, enhanced the severity of ventricular arrhythmias as shown by a significant dose-dependent increase in the number of ventricular ectopic beats, duration of ventricular tachycardia (VT) and ventricular fibrillation (VF). This effect was antagonized by pretreatment with the selective 5-HT2-receptor antagonist ritanserin (1 mg kg-1, i.p.) given 15 minutes before 5-HT. Ritanserin when used alone was observed to produce a significant reduction in the number of ventricular ectopic beats and duration of VT and VF. 5-HT significantly lowered the heart rate and produced initial rise of the systolic blood pressure (SBP). These effects were antagonized by ritanserin. Ritanserin significantly lowered the heart rate but did not alter the SBP. It was postulated that 5-HT might be implicated in the genesis and determination of severity of ventricular arrhythmias induced by acute myocardial ischemia, and that this effect is mediated via 5-HT2-receptors. 5-HT2-receptor antagonists may provide potential useful therapeutic agents for the management of these arrhythmias.

J Cardiovasc Electrophysiol. 2003 Feb;14(2):209-14.
5-hydroxytryptamine and atrial fibrillation: how significant is this piece in the puzzle?
Yusuf S, Al-Saady N, Camm AJ.
5-Hydroxytryptamine, a recent addition to the list of hormonal triggers for atrial fibrillation (AF), may play a pivotal role in the induction of AF related not only to cardiac surgery but also to acute coronary syndromes, valvular heart disease, cardiomyopathies, alcoholism, aging, and conducting tissue disease. This review examines the supporting laboratory and clinical evidence and provides a comprehensive insight into the basic underlying mechanisms involved. It also delves into the potential benefits and limitations of 5-HT4 antagonists in the prevention and management of this arrhythmia.

Psychosomatics. 2006 Nov-Dec;47(6):533-6.
Cardioversion of persistent atrial arrhythmia after treatment with venlafaxine in successful management of major depression and posttraumatic stress disorder
Finch SJ, van Zyl LT.
There is increasing evidence linking depression and cardiovascular disease. However, the authors could find no literature directly linking depression with atrial fibrillation or atrial flutter. The authors report the case of a patient with uncontrolled atrial arrhythmia who cardioverted to normal sinus rhythm after treatment of major depressive disorder (MDD) and posttraumatic stress disorder (PTSD) with venlafaxine. The authors discuss comorbidity of MDD and atrial fibrillation, and explore evidence of venlafaxine as an antiarrhythmic agent. Further research is needed to establish the clinical role of venlafaxine as a Class 1 antiarrhythmic agent and any association between atrial arrhythmias and MDD and PTSD.

Clin Res Cardiol. 2007 Feb;96(2):114-8.
Atrial fibrillation in carcinoid heart disease: The role of serotonin. A review of the literature.
Langer C, Piper C, Vogt J, Heintze J, Butz T, Lindner O, Burchert W, Kersting C,
Horstkotte D.

J Mol Cell Cardiol. 2007 Jan;42(1):51-3.
5-hydroxytryptamine and atrial arrhythmogenesis: a “culprit mechanism” or bystander in patients with chronic atrial fibrillation?
Dobrev D.

43. Indian J Physiol Pharmacol. 1973 Apr-Jun;17(2):111-6.
Influence of 5-hydroxytryptamine on experimentally induced atrial arrhythmias in dogs.
Kuruvilla A, Aiman R.

Sov Med. 1972 Oct;35(10):30-3.
[Some aspects of the metabolism of biogenic monoamines (catecholamines and serotonin) in fibrillation arrhythmia treated by electrical impulses].
[Article in Russian]
Berestov AA, Safronova VI.

Klin Med (Mosk). 1971 Jan;49(1):25-9.
[Blood serotonin content during auricular fibrillation and its treatment by defibrillation].
[Article in Russian]
Panchenko VM, Kucherenko IA.

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“Selye’s demonstration of corn oil’s toxicity to the heart is an important link in the general picture of stress injury and adrenalin toxicity. The protective effects of saturated fats are not surprising when seen against the background of the toxic effects of adrenalin, causing the mobilization of fatty acids and the resulting lipid peroxidation.”

PUFA and arrhythmia:
Cardiovasc Res. 2007 Jan 15;73(2):386-94. Epub 2006 Oct 13.
Dietary n-3 fatty acids promote arrhythmias during acute regional myocardial ischemia in isolated pig hearts.
Coronel R, Wilms-Schopman FJ, Den Ruijter HM, Belterman CN, Schumacher CA, Opthof T, Hovenier R, Lemmens AG, Terpstra AH, Katan MB, Zock P.
OBJECTIVE:
Dietary supplementation with fish oil-derived n-3 fatty acids reduces mortality in patients with myocardial infarction, but may have adverse effects in angina patients. The underlying electrophysiologic mechanisms are poorly understood. We studied the arrhythmias and the electrophysiologic changes during regional ischemia in hearts from pigs fed a diet rich in fish oil.
METHODS:
Pigs received diets rich in fish oil, in sunflower oil, or a control diet for 8 weeks. Hearts were isolated and perfused. Ischemia was created by occluding the left anterior descending artery. Diastolic stimulation threshold, refractory period, conduction velocity, activation recovery intervals and the maximum downstroke velocity of 176 electrograms were measured in the ischemic zone. Spontaneous arrhythmias during 75 min of regional ischemia were counted.
RESULTS:
More episodes of spontaneous ischemia-induced sustained ventricular tachycardia and ventricular fibrillation occurred in the fish oil and sunflower oil group than in the control group. More inexcitable myocardium was present in the ischemic zone in the group fed fish oil or sunflower oil than in the control group after 20 min of ischemia. After 40 min of ischemia, more block occurred in the control group than in the other groups. The downstroke velocity of the electrograms in the ischemic border zone was lower in the fish oil group and sunflower oil group than in the control after 20 min.
CONCLUSIONS:
A diet rich in fish oil results in proarrhythmia compared to a control diet during regional ischemia in pigs. Myocardial excitability is reduced in the fish oil and sunflower oil group during the early phase of arrhythmogenesis. In the late phase of arrhythmogenesis, excitability is more reduced in the control group than in the fish oil and sunflower oil group.

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Progesterone protects against hemorrhagic shock, improves cardiovascular responses:

Crit Care Med. 2003 Jun;31(6):1786-93.
Progesterone administration after trauma and hemorrhagic shock improves cardiovascular responses.
Kuebler JF1, Jarrar D, Bland KI, Rue L 3rd, Wang P, Chaudry IH.
OBJECTIVE:
Studies have shown that female rats during the proestrus stage have significantly improved cell and organ functions after trauma-hemorrhage compared with male and ovariectomized females. This study investigated the hypothesis that progesterone can improve the depressed cardiovascular function in sex steroid-deficient female rats (i.e., ovariectomized females) after trauma-hemorrhage and resuscitation.
DESIGN:
Prospective study.
SETTING:
University laboratory.
SUBJECTS:
Ovariectomized female Sprague-Dawley rats (weight, 250-300 g).
INTERVENTIONS:
Rats underwent a 5-cm midline laparotomy (i.e., soft-tissue trauma), were bled to a mean arterial pressure of 35 mm Hg for approximately 90 mins, and were then resuscitated using Ringer’s lactate. A single dose of progesterone (25 mg/kg of body weight) or vehicle was administered subcutaneously during resuscitation.
MEASUREMENTS:
At 20 hrs after trauma-hemorrhage or sham operation, cardiac output and heart performance and the circulating blood volume were assessed using the indocyanine green dilution technique and a left ventricular catheter. Furthermore, the binding activity of progesterone receptors in nuclear extracts of left ventricular tissue was determined.
RESULTS:
Cardiac output, heart performance, and circulating blood volume were significantly decreased in vehicle-treated animals after trauma-hemorrhage. Administration of progesterone significantly improved cardiac output and heart performance and increased the circulating blood volume. This was associated with an increased progesterone receptor activity in the left ventricular nuclear extracts.
CONCLUSION:
Because administration of progesterone after trauma-hemorrhage in sex steroid-deficient females improved cardiovascular responses, this hormone seems to be a useful adjunct for the treatment of cardiovascular depression in postmenopausal and ovariectomized female trauma patients.

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By Team FPS – December 20, 2012

Lactose Intolerance: Starch, Fructose, Sucrose, & Thyroid Status

Also see:
Hypothyroidism, Intestinal Bacterial Overgrowth, & Lactose Intolerance
Autoimmunity and Intestinal Flora
Thumbs Up: Fructose

Am J Physiol. 1995 Jun;268(6 Pt 1):G1066-73.
Diet-induced changes in gene expression of lactase in rat jejunum.
Goda T, Yasutake H, Suzuki Y, Takase S, Koldovský O.
To explore the mechanisms by which jejunal lactase activity is modified by carbohydrate and/or fat intake, mRNA levels and the absolute synthesis rate of lactase-phlorizin hydrolase (LPH) were determined in 6-wk-old rats that were fed either low-starch diets containing long-chain triacylglycerol (LCT, 73% energy as corn oil) or medium-chain triacylglycerol (MCT, 66% energy as MCT, 7% energy as corn oil), or a high-starch diet (70% energy as cornstarch) for 7 days. LPH mRNA levels in the jejunum were similar between LCT-fed and MCT-fed rats, but animals fed the high-starch diet exhibited a greater (2x) LPH mRNA level than other groups. The absolute synthesis rate of LPH, estimated by the flooding dose technique using [3H]phenylalanine, was greater (2.4x) in rats fed the high-starch diet than in other groups. A short-term force-feeding experiment revealed that sucrose was able to evoke LPH mRNA levels within 12 h but that a nonmetabolizable sugar (alpha-methylglucoside) was unable to enhance it. By contrast, animals fed the high-LCT diet showed a lower (by 30%) lactase activity than rats fed the low-starch, high-MCT diet, which was accompanied by not only a reduction of immunoreactive LPH in brush-border membranes but also a reduction in lactase activity per unit weight of immunoreactive LPH. These results suggest that both gene expression and posttranslational events of LPH might be influenced by dietary manipulations; carbohydrate intake primarily increases LPH mRNA levels, and LCT accelerates inactivation and/or degradation of lactase.

Biochem J. 1998 Apr 1;331 ( Pt 1):225-30.
Dietary carbohydrates enhance lactase/phlorizin hydrolase gene expression at a transcription level in rat jejunum.
Tanaka T, Kishi K, Igawa M, Takase S, Goda T.
We have previously shown that dietary sucrose stimulates the lactase/phlorizin hydrolase (LPH) mRNA accumulation along with a rise in lactase activity in rat jejunum [Goda, Yasutake, Suzuki, Takase and Koldovský (1995) Am. J. Physiol. 268, G1066-G1073]. To elucidate the mechanisms whereby dietary carbohydrates enhance the LPH mRNA expression, 7-week-old rats that had been fed a low-carbohydrate diet (5.5% of energy as starch) were given diets containing various monosaccharides or sucrose for 12h. Among carbohydrates examined, fructose, sucrose, galactose and glycerol elicited an increase in LPH mRNA accumulation along with a rise in lactase activity in the jejunum. By contrast, glucose and alpha-methylglucoside were unable to elicit a significant increase in LPH mRNA levels. To explore a transcriptional mechanism for the carbohydrate-induced increases in LPH mRNA levels, we employed two techniques currently available to estimate transcriptional rate, i.e. RNA protection assays of pre-mRNA using an intron probe, and nuclear run-on assays. Both assays revealed that fructose elicited an increase in transcription of the LPH gene, and that the transcription of LPH was influenced only slightly, if at all, by glucose intake. These results suggest that certain monosaccharides such as fructose or their metabolite(s) are capable of enhancing LPH mRNA levels in the small intestine, and that transcriptional control might play a major role in the carbohydrate-induced increase of LPH mRNA expression.

J Nutr Sci Vitaminol (Tokyo). 2006 Oct;52(5):347-51.
Dietary sucrose enhances intestinal lactase gene expression in euthyroid rats.
Kuranuki S, Mochizuki K, Goda T.
It is postulated that dietary carbohydrates and thyroid hormones are major regulators for expression of the lactase/phlorizin hydrolase (LPH) gene in rat jejunum. In this study, we investigated the effects of thyroid hormones and dietary sucrose on LPH gene expression and lactase activity in starved rats. Firstly, animals at 8 wk of age were fed a low-starch diet (5.5% energy as cornstarch) or high-starch diet (71% energy as cornstarch) for 7 d (experiment 1). The mRNA level of LPH as well as lactase activity significantly decreased in rats fed the low-starch diet as compared to those fed the high-starch diet. To investigate the effects of thyroid hormone status, the animals previously fed the low-starch diet were starved for 3 d, and half of the animals were given intraperitoneal (i.p.) injections of 20 microg/ 100 g body weight triiodothyronine (T3) twice daily (experiment 2). The LPH mRNA level and lactase activity were elevated by starvation for 3 d, but they were repressed by the injection of T3 during starvation. To investigate the effects of dietary sucrose in starved rats, they were force-fed a sucrose diet for 6 h (experiment 3). The LPH gene expression and lactase activity were up-regulated by force-feeding a sucrose diet, only when the animals were kept in euthyroid status by daily T3 administrations. In contrast, the sucrase-isomaltase mRNA levels and sucrase activity were unaffected by force-feeding the sucrose diet for both T3-treated and untreated starved rats. Our work suggests that dietary sucrose is capable of enhancing lactase gene expression in starved rats when they have a sustainable thyroid hormone level.

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By Team FPS – December 19, 2012

How Vegetable Oils Replaced Animal Fats in the American Diet

In this excerpt from The Happiness Diet, discover how Procter & Gamble convinced people to forgo butter and lard for cheap, factory-made oils loaded with trans fat.

Book ExcerptBefore highways and before railroads, America conducted her commerce via steamship over water through a system of rivers, canals, and lakes. In the 1800s, Cincinnati was the heart of the developed United States. At the time it was known to the world as Porkopolis. That’s because not so long ago, the most widely consumed meat in this nation was swine. 

This was before refrigeration. The biggest enemy of 19th-century butchers was spoilage. Eating cows didn’t make a whole lot of sense: Distributing the meat of a freshly killed 1,500-pound animal before it went bad was difficult without roads and temperature-controlled trains. But pigs are fatty, which makes them excellent for salt curing because they don’t lose flavor.

Cincinnati is on the Ohio River, which flows to the Mississippi River, which leads to the ever-important port of New Orleans. From the mouth of the mighty Mississippi, Porkopolis distributed meat throughout the coastal southern United States. The by-products of pork production meant that the burgeoning metropolis was also home to many tanneries, boot makers, and upholsters. Animal fats were hot commodities, as they were rendered and molded into soap and candles. Breaking down pigs was a highly efficient process known as the disassembly line — an idea that would later be reverse-engineered by Henry Ford to produce automobiles.

A major economic depression in the 1870s caused two important citizens of Porkopolis to join forces in order to cut costs and survive the bear market. They formed a company that would eventually be responsible for the greatest dietary shift in our country’s history. William Procter brought his candle-making business to the states after a fire destroyed his business in England. James Gamble fled Ireland during the Great Potato Famine and became a soap manufacturer. In a twist of fate, the two men happened to marry sisters in Cincinnati. Together, the brothers-in-law formed Procter & Gamble, a soap- and candle-manufacturing operation.

“What was garbage in 1860 was fertilizer in 1870, cattle feed in 1880, and table food and many things else in 1890.” — Popular Science, on cottonseed

At the time, soap was sold in huge wheels that were sliced into custom-sized portions at general stores. Procter and Gamble decided to take a chance by mass-producing individually wrapped bars of soap. To pull this off, the brother-in-laws needed to drastically reduce the price of their raw ingredients, which meant finding a replacement for expensive animal fats. They settled on a mix of palm and coconut oils and created the first soap that floated in water — a handy invention when clothes and dishes alike were washed in a sudsy basin. Hard pressed to come up with a name for this new product, Procter looked to the bible for inspiration and found it in Psalm 45:8: “All thy garments smell of myrrh, and aloes, and cassia, out of the ivory palaces, whereby they have made thee glad.” The word Ivory was trademarked, and in short order Americans all over the country would know the purity of this soap.

Oddly enough, the company to thank for the fact that America now eats so much vegetable oil has never produced much in the way of food. Thanks to Procter & Gamble the United States boosted the production of a waste product of cotton farming, cottonseed oil. To ensure a steady, cheap supply for soap production the company formed a subsidiary in 1902 called Buckeye Cotton Oil Co. Before processing, cottonseed oil is cloudy red and bitter to the taste because of a natural phytochemical called gossypol (it’s used today in China as male birth control) and is toxic to most animals, causing dangerous spikes in the body’s potassium levels, organ damage, and paralysis.

An issue of Popular Science from the era sums up the evolution of cottonseed nicely: “What was garbage in 1860 was fertilizer in 1870, cattle feed in 1880, and table food and many things else in 1890.” But it entered our food supply slowly. It wasn’t until a new food-processing invention of hydrogenation that cottonseed oil found its way into the kitchens of America’s restaurants and homes.

Edwin Kayser, a German chemist, wrote to Procter & Gamble on October 18, 1907, about a new chemical process that could create a solid fat from a liquid. The company’s researchers had been interested in producing a solid form of cottonseed oil for years, and Kayser described his new process as “of the greatest possible importance to soap manufacturers.” The company purchased US rights to the patents and created a lab on the Procter & Gamble campus, known as Ivorydale, to experiment with the new technology. Soon the company’s scientists produced a new creamy, pearly white substance out of cottonseed oil. It looked a lot like the most popular cooking fat of the day: lard. Before long, Procter & Gamble sold this new substance (known today as hydrogenated vegetable oil) to home cooks as a replacement for animal fats.

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Procter & Gamble filed a patent application for the new creation in 1910, describing it as “a food product consisting of a vegetable oil, preferably cottonseed oil, partially hydrogenated, and hardened to a homogeneous white or yellowish semi-solid closely resembling lard. The special object of the invention is to provide a new food product for a shortening in cooking.” They came up with the name Crisco, which they thought conjured up crispness, freshness, and cleanliness.

Convincing homemakers to swap butter and lard for a new fat created in a factory would be quite a task, so the new form of food needed a new marketing strategy. Never before had Procter & Gamble — or any company for that matter — put so much marketing support or advertising dollars behind a product. They hired the J. Walter Thompson Agency, America’s first fullservice advertising agency staffed by real artists and professional writers. Samples of Crisco were mailed to grocers, restaurants, nutritionists, and home economists. Eight alternative marketing strategies were tested in different cities and their impacts calculated and compared. Doughnuts were fried in Crisco and handed out in the streets. Women who purchased the new industrial fat got a free cookbook of Crisco recipes. It opened with the line, “The culinary world is revising its entire cookbook on account of the advent of Crisco, a new and altogether different cooking fat.” Recipes for asparagus soup, baked salmon with Colbert sauce, stuffed beets, curried cauliflower, and tomato sandwiches all called for three to four tablespoons of Crisco.

Health claims on food packaging were then unregulated, and the copywriters claimed that cottonseed oil was healthier than animal fats for digestion. Advertisements in the Ladies’ Home Journal encouraged homemakers to try the new fat and “realize why its discovery will affect every family in America.” The unprecedented product rollout resulted in the sales of 2.6 million pounds of Crisco in 1912 and 60 million pounds just four years later. This new food bolstered the bottom line of a company whose other products were Ivory Soap, Lenox Soap, White Naphtha Laundry Soap, and Star Soap. It also helped usher in the age of margarine as well as low-fat foods.

Procter & Gamble’s claims about Crisco touching the lives of every American proved eerily prescient. The substance (like many of its imitators) was 50 percent trans fat, and it wasn’t until the 1990s that its health risks were understood. It is estimated that for every two percent increase in consumption of trans fat (still found in many processed and fast foods) the risk of heart disease increases by 23 percent. As surprising as it might be to hear, the fact that animal fats pose this same risk is not supported by science.

Reprinted from The Happiness Diet (c) 2011 by Drew Ramsey, MD and Tyler Graham. Permission granted by Rodale, Inc. Available wherever books are sold.

 

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By Team FPS – December 13, 2012

Hypothyroidism Causes Shrinking of the Thymus Gland

Hypothyroidism causes the thymus gland to atrophy (Abou-Rabia and Kendall, 1994), partly because the thyroid hormone itself is essential for the maintenance of the gland, and also because hypothyroidism is likely to be accompanied by excessive levels of estrogen and cortisol. -Ray Peat, PhD

Cell Tissue Res 1994 Sep;277(3):447-SS.
Involution of the rat thymus in experimentally induced hypothyroidism.
AbouRabia N, Kendall MD.
The thymus, as part of the immune-neuroendocrine axis, is greatly influenced by factors from most endocrine glands, especially the thyroid. Antithyroid drugs (carbimazole and methimazole) were used to induce hypothyroidism in rats. Histological and ultrastructural examination of the thymus showed progressive thymic involution after 4 weeks of drug treatment to the end of observations (7 weeks). The involution was characterised by increased thymocyte apoptosis and thymocyte phagocytosis by macrophages. This resulted in thymocyte depopulation, increases in numbers of interdigitating cells, alterations to mainly subcapsular and medullary epithelial cells, an apparent increase of mast cells and collagen in the capsule and septa, and increased numbers of B cells and plasma cells. Lymphoid cells immuno-reactive with MRC OX12 (which detects B cells) were observed within blood vessel walls, suggesting that they may have been moving in and out of the thymus. The administration of drugs causing hypothyroidism, therefore, also caused marked involution of the thymus.

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By Team FPS – December 12, 2012

Protected: Shut Your Mouth and Save Your Life

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By Team FPS – December 9, 2012