Considering the amount of time and money people spend on how they look, I think it’s reasonable to say that the pursuit of physical attractiveness has become a lifestyle. Most people want to be good looking, especially to whom they find attractive. The desire for beauty is probably healthy and natural, and in some peoples’ minds, may represent noble aspirations, such as the desire to manifest oneself as the highest expression of his or her physical being.
People will do anything to their bodies in the pursuit of physical attractiveness: they will pierce it, tattoo it, keep it in shape by exercising and dieting, and if they don’t like a part of their body, they will have surgery to reduce or augment it.
Contrary to popular opinion, physical attractiveness is not merely “skin deep”; nor is it the prerogative of those who are seemingly genetically endowed. Rather, it is determined by the conditions that are available to us, which are, more or less, governed by the state of our digestion, rate of metabolism, immune system status, and perceived stress levels. Physical attractiveness appears to be a real indicator of genetic and developmental health (Cunningham, Barbee, & Pike, 1990), and furthermore, we can employ the view that people have of attractive people – that they are more socially competent, intelligent, interesting, and friendly than people who are unattractive - to support this holistic view.
Although there are subtle differences between cultures, symmetry and youthfulness are universal standards of physical attractiveness. These are traits that diminish with aging (Apicella, Little, & Marlowe, 2007; Little, Apicella, & Marlowe, 2007).
Concerning guys, slightly feminized features appear to increase the ranking of their physical appearance to the opposite sex (Perrett et al. 1998). Women, however, have been shown to have stronger preferences for more masculine features during periods in their menstrual cycles when estrogen levels are high (Roney & Simmons, 2008). . . . Testosterone levels predict the preference for masculine and feminine traits for women and men, respectively (Welling et al., 2007).
Believe it or not, facial symmetry can fluctuate over time, albeit subtly. These changes are executed through genomic recombination, and are governed by the severity and aggregate of stressors encountered by an individual in his or her lifetime. In fact, symmetry of bilateral features is a valid and reliable marker of the stresses (genetic and environmental) encountered by organisms across taxa.
Symmetry of facial features is universally aesthetic, and now we know why this is the case. In a way, symmetry of bilateral traits “monitors” the physiological and metabolic ravages of stresses, and therefore, an individual’s overall “fitness”. Facial symmetry, for instance, is a valid marker of cognitive aging in males, and, individuals with Down’s syndrome, who serve as models of genomic instability, present with fluctuating dental asymmetry (Barden, 1980; Penke et al., 2009).
When energy production slows, especially in the face of stresses, reactive oxygen species (ROS) are produced in large amounts. With aging, the cumulative damages to respiratory complex proteins in the mitochondria, e.g., cytochrome c oxidase, by ROS ultimately leads to metabolic rate slowing, diminished metabolic stability, and a low efficiency of oxidative metabolism.
Taking antioxidants in large amounts, per se, such as vitamin c, is unnecessary, and could be harmful, as the endoplasmic reticulum, which is where a large part of oxidative stress/damage originates, requires an oxidative environment to function properly. Correcting nutritional deficiencies, lowering nonesterified fatty acids (NEFA) levels, and eradicating overstuffed fat cells are more rational courses of action to preserve a high rate of metabolism and to prevent the continual activation of the degenerative unfolded protein response.
Possibly a topic for another post, but energy, namely, ATP, serves as the principle cardinal adsorbent in all cells, and allows for cells to “organize” its water and structural elements properly. In other words, ATP is synonymous with life, and anything that diminishes it, such as forced fatty acid burning/glycolysis, diminishes our life force.
I think metabolic derangements associated with endotoxemia are at the core of the aging process. Endotoxemia is caused by gut bacteria that possess a toxic outer cell-wall component called lipopolysaccharide (LPS). Unlike other bacterial toxins, LPS is not secreted, but instead, released by bacteria upon being destroyed or killed. Under certain conditions, LPS can “slip” through the intestinal barrier, subsequently reaching the bloodstream, where upon coming into contact with pathogen recognizing proteins on cells, found in tissues throughout the body, can activate inflammatory pathways.
Obese individuals have high circulating levels of LPS. LPS mainly interacts with pathogen recognizing proteins on immune system cells, such as macrophages, and in doing so, increases the expression of the transcription factor, NF- κB, which in turn, turns on a host of genes related to inflammation and aging – particularly skin aging (Adler et al., 2007).
Premature fat cells, in many ways, behave like immune system cells in that upon coming into contact with LPS, produce inflammatory adipokines that interfere with fat cell differentiation and division (hyperplasia) (Suganami, Nishida, & Ogawa, 2005). The failure of premature fat cells to mature leads to a large population of young and overstuffed fat cells (hypertrophy). This initiates the path to “pathogenic obesity”. . . .
Downstream of TLR and NF- κB activation, LPS increases the expression of cyclooxygenase-2, and, via TNF-α, activates the inducible nitric oxide synthase, increasing the production of a reactive gas called nitric oxide. Nitric oxide, by way of phosphorylation, increases the activity of the enzyme hormone sensitive lipase in fat cells. As a result, fatty acids, mostly palmitate, are released in droves into the bloodstream (Staiger et al., 2004). TNF-α and fatty acids act on the same pathogen recognizing protein that LPS does, representing a vicious cycle whereby the inflammatory state initiated by LPS is reinforced and amplified.
Diabetics show high circulating LPS levels at rest and after meals . . . which is to be expected, as diabetes is characterized by low-grade inflammation and expanded fat cells. The conditions produced under the exposure to LPS lead to insulin resistance in the body through the release of fatty acids and inflammatory cytokines by pathogenic fat tissue (Lien, Au, Tsai, Ho, & Juan, 2009).
Some diabetes drugs are effective because they, one way or another, act on the pathways affected by LPS. For instance, thiazolidinediones promote adipocyte differentiation, and as a result, curtail the development of pathogenic fat tissue (Lehmann et al., 1995).
Observational studies have shed light on the association between diet and endotoxemia. We can provisionally regard starch/glucose, fat, and high-energy meals to be the worst offenders based on a series of experiments published by Ghanim et al. and others (e.g., Erridge, Attina, Spickett, & Webb, 2007). Fruit and fructose on the other hand do not increase LPS levels, and, in ways that have yet to be fully explained, can prevent the LPS increasing effect of the previously mentioned foods (Ghanim et al., 2010).
LPS not only binds the transmembrane protein, TLR-4, but also to endogenous substances produced during inflammation, such as NEFA. An important distinction lies in the types of inflammation produced in that endogenous ligands result in low-grade, chronic inflammation, whereas exogenous ligands result in high-grade, acute inflammation. Though, often both are occurring simultaneously.
TLR-4, which actually binds to a range of microbial components, also increases the expression of TLR-2, thereby allowing components derived from gram-positive bacteria to elicit degenerative processes, like TLR-4 activation does. TLR-2 increases the expression of IL-6 that among other things decreases a protective fat-derived hormone called adiponectin, contributing further to the dysregulated pattern of hormones secreted by adipose tissue.
Experiments in which mice are engineered to not express TLR are protected from high-fat diet induced obesity, insulin resistance, and inflammation (Davis, Gabler, Walker-Daniels, & Spurlock, 2008; Suganami et al., 2007).
By reducing the intestinal bacterial load, antibiotics, too, provide protection against LPS and the associated sequelae in obese and high-fat diet fed mice (Cani et al., 2008). Along the same lines minimizing dietary soluble fiber keeps bacterial proliferation in check.
The avoidance of large meals and excessive dietary fat, by decreasing intestinal permeability, inhibits the post-meal rise of LPS; the rise of NEFA is blunted as well.
Weight loss, in itself, decreases NEFA and LPS levels at rest and after meals. Consequently, pathogenic fat cells revert to their normal phenotype with a concomitant decrease in inflammation. Insulin levels decrease, too, which explains, in part, the positive changes in non-adipose tissue membrane fatty acid composition.
The saturation index of membrane lipids is under the control of insulin (among other things). So under certain circumstances, the saturation index of membrane lipids in non-adipose tissue stays relatively constant, regardless of the diet. Calorie restriction is associated with a higher membrane saturation index and stability, which is a significant reason why this practice increases lifespan in animals. Conversely, upregulation of the desaturation enzymes is linked to diseases, including cancer (Roongta et al., 2011).
Adipose tissue fatty acids, which are stored as triglycerides, reflect an individual’s dietary fat intake near perfectly. NEFA are mostly derived from adipose tissue triglycerides, so in this sense, the types of dietary fat consumed is an important consideration. Monounsaturated fats and saturated fats (namely, short and medium chain) are ideal in this respect in that they flow down the ω-9 synthetic pathway, rather than ω-6 or ω-3, resulting in polyunsaturated fatty acids with three or four double bonds, instead of five or six.
A lower saturation index goes along with a greater amount of fatty acid substrates that bend into a U shape for eicosanoid synthesis, e.g., arachidonic acid. As previously put forth, cycloxoygenase-2 is one of the gene products upregulated by LPS. The upregulation of cyclooxygenase-2 is associated with breast cancer in mammals (Brodie et al., 2001).
Taken together, maintaining a high muscle-to-fat ratio, as well as a high saturation index, reasonable quantities of fat-soluble antioxidants, low NEFA levels, and avoiding the dietary factors that increase bacterial proliferation and intestinal permeability allows us to deal with stresses, really, of any kind in a timely and innocuous manner, which in turn, preserves our youth and the things that make us physically attractive to others.
People will do extreme things to their bodies in the pursuit of beauty and youth. However, the measures undertaken are often misguided and to no avail. Aging and physical attractiveness are governed by well-defined metabolic derangements – a signature of sorts – which are amenable to specific dietary and pharmacological interventions. . . . as long as they are initiated early enough.
This post is a bit off the beaten path from my usual fare but rest assured, because it will be back to the usual stuff from hereon in.
Considering the enormity of this topic, only a few key points were discussed in this post; perhaps I will continue. . . . If this one generates enough interest, of course.
References
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