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An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity
The Center for Genetics, Nutrition and Health, 4330 Klingle Street NW, Washington, DC 20016, USA
Nutrients 2016, 8(3), 128; https://doi.org/10.3390/nu8030128
Received: 15 January 2016 / Revised: 10 February 2016 / Accepted: 15 February 2016 / Published: 2 March 2016
(This article belongs to the Special Issue Fatty Acids in Obesity and Type 2 Diabetes)
In the past three decades, total fat and saturated fat intake as a percentage of total calories has continuously decreased in Western diets, while the intake of omega-6 fatty acid increased and the omega-3 fatty acid decreased, resulting in a large increase in the omega-6/omega-3 ratio from 1:1 during evolution to 20:1 today or even higher. This change in the composition of fatty acids parallels a significant increase in the prevalence of overweight and obesity. Experimental studies have suggested that omega-6 and omega-3 fatty acids elicit divergent effects on body fat gain through mechanisms of adipogenesis, browning of adipose tissue, lipid homeostasis, brain-gut-adipose tissue axis, and most importantly systemic inflammation. Prospective studies clearly show an increase in the risk of obesity as the level of omega-6 fatty acids and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane phospholipids, whereas high omega-3 RBC membrane phospholipids decrease the risk of obesity. Recent studies in humans show that in addition to absolute amounts of omega-6 and omega-3 fatty acid intake, the omega-6/omega-3 ratio plays an important role in increasing the development of obesity via both AA eicosanoid metabolites and hyperactivity of the cannabinoid system, which can be reversed with increased intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). A balanced omega-6/omega-3 ratio is important for health and in the prevention and management of obesity.
1. Introduction
Obesity is a complex condition involving the dysregulation of several organ systems and molecular pathways, including adipose tissue, liver, pancreas, gastrointestinal tract, the microbiome, the central nervous system (CNS), and genetics. The role of the CNS in obesity is receiving more attention as obesity rates rise and treatments continue to fail. While the role of the hypothalamus in the regulation of appetite and food intake has long been recognized, the roles of the CNS reward systems are beginning to be examined as the role of environmental influences on energy balance are explored. Furthermore, omega-3 fatty acids hold great promise in the prevention and management of obesity.
Omega-6 and omega-3 polyunsaturated fatty acids (PUFAs) are essential fatty acids that must be derived from the diet, cannot be made by humans, and other mammals because of the lack of endogenous enzymes for omega-3 desaturation [1,2]. Due to agribusiness and modern agriculture western diets contain excessive levels of omega-6 PUFAs but very low levels of omega-3 PUFAs, leading to an unhealthy omega-6/omega-3 ratio of 20:1, instead of 1:1 that was during evolution in humans (Figure 1) [1,3].
Eicosanoid products derived from omega-6 PUFAs (such as prostaglandin (PG) E2 and leukotriene (LT) B4 synthesized from arachidonic acid (AA)) are more potent mediators of thrombosis and inflammation than similar products derived from omega-3 PUFAs (PGE3 and LTB5 synthesized from eicosapentaenoic acid (EPA)) (Figure 2) (Table 1) [1,2,3].
Thus, an unbalanced omega-6/omega-3 ratio in favor of omega-6 PUFAs is highly prothrombotic and proinflammatory, which contributes to the prevalence of atherosclerosis, obesity, and diabetes [1,2,3,4,5,6]. In fact, regular consumption of diets rich in omega-3 PUFAs have been associated with low incidence of these diseases, particularly in Icelandic populations, Inuit indigenous people, and Native Americans in Alaska [7,8,9]. However, using fish oil as the primary source of omega-3 PUFAs to treat type 2 diabetes has not always met with success [6,10,11]. Although nutritional studies suggest that high omega-6/omega-3 ratios have contributed significantly to the "obesity epidemic" [12,13], clinical trials using omega-3 PUFAs as weight-reducing agents have produced conflicting findings of both positive [14,15,16] and negative effects [17,18,19] due to many factors (Table 2).
This paper focuses, on the differential aspects of omega-6 and omega-3 fatty acids and their ratio, in energy balance and in the prevention and management of obesity.
2. The Importance of the Omega-6/Omega-3 Fatty Acid Ratio: Metabolic, Physiological and Evolutionary Aspects
There are two classes of essential fatty acids (EFA), omega-6 and omega-3. The distinction between omega-6 and omega-3 fatty acids is based on the location of the first double bond, counting from the methyl end of the fatty acid molecule. Omega-6 fatty acids are represented by linoleic acid (LA) (18:2ω-6) and omega-3 fatty acids by alpha-linolenic acid (ALA) (18:3ω-3). LA is plentiful in nature and is found in the seeds of most plants except for coconut, cocoa, and palm. ALA, on the other hand, is found in the chloroplasts of green leafy vegetables, and in the seeds of flax, rape, chia, perilla and walnuts. Both essential fatty acids are metabolized to longer-chain fatty acids of 20 and 22 carbon atoms. LA is metabolized to arachidonic acid (AA) (20:4ω6) while ALA is metabolized to eicosapentaenoic acid (EPA) (20:5ω3) and docosahexaenoic acid (DHA) (22:6ω3). This is achieved by increasing the chain length and the degree of unsaturation by adding extra double bonds to the carboxyl end of the fatty acid molecule [20] (Figure 3). AA is found predominantly in the phospholipids of grain-fed animals, dairy and eggs. EPA and DHA are found in the oils of fish, particularly fatty fish.
In mammals, including humans, the cerebral cortex, retina, testis and sperm are particularly rich in DHA. DHA is one of the most abundant components of the brain's structural lipids. DHA, like EPA, can be derived only from direct ingestion or by synthesis from dietary EPA or ALA: humans and other mammals, except for certain carnivores such as lions, can convert LA to AA and ALA to EPA and DHA, although the process is slow [21,22]. There is competition between omega-6 and omega-3 fatty acids for the desaturation enzymes. Both fatty acid desaturase 1 (FADS1) and fatty acid desaturase 2 (FADS2) prefer ALA to LA [21,23,24]. However a high LA intake, such as that characterizing Western diets, interferes with the desaturation and elongation of ALA [22,23,24,25]. Similarly, trans fatty acids interfere with the desaturation and elongation of both LA and ALA.
There are important genetic variables in fatty acid biosynthesis involving FADS1 and FADS2, which encode rate-limiting enzymes for fatty acid metabolism (Figure 3). Ameur et al. [26] performed genome-wide genotyping (n = 5652 individuals) of the FADS region in five European population cohorts and analyzed available genomic data from human populations, archaic hominins, and more distant primates. Their results show that present-day humans have two common FADS haplotypes A and D that differ dramatically in their ability to generate long-chain polyunsaturated fatty acids (LC-PUFAs). The most common haplotype, denoted haplotype D, was associated with high blood lipid levels (p = 1 × 10−65), whereas the less common haplotype (haplotype A) was associated with low blood lipid levels (p = 1 × 10−52). The haplotype D associated with the enhanced ability to produce AA and EPA from their precursors LA and ALA respectively is specific to humans and has appeared after the split of the common ancestor of humans and Neanderthals. This haplotype shows evidence of a positive selection in African populations in which it is presently almost fixed and it is less frequent outside of Africa. Haplotype D provides a more efficient synthesis of LC-PUFAs and in today's high LA omega-6 dietary intake from vegetable oils, it leads to increased synthesis of AA from LA. As a result Haplotype D represents a risk factor for coronary heart disease (CHD), cancer, obesity, diabetes and the metabolic syndrome, adding further to health disparities in populations of African origin living in the West, in addition to lower socioeconomic status [27,28]. Furthermore, FADS2 is the limiting enzyme and there is some evidence that it decreases with age [21]. Premature infants [29], hypertensive individuals [30], and some diabetics [31] are limited in their ability to make EPA and DHA from ALA. These findings are important and need to be considered when making dietary recommendations. Genetic variants in FADS cluster are determinants of long-chain PUFA levels in circulation, cells and tissues. These genetic variants have been studied in terms of ancestry, and the evidence is robust relative to ethnicity. Thus, 80% of African Americans and about 45% of European Americans carry two copies of the alleles associated with increased levels of AA. It is quite probable that gene PUFA interactions induced by the modern Western diet are differentially driving the risk of diseases of inflammation (obesity, diabetes, atherosclerosis and cancer) in diverse populations.
As mentioned earlier, mammalian cells cannot convert omega-6 to omega-3 fatty acids because they lack the converting enzyme, omega-3 desaturase. Omega-6 and omega-3 fatty acids are not interconvertible, are metabolically and functionally distinct, and often have important opposing physiological effects, therefore their balance in the diet is important. When humans ingest fish or fish oil, the EPA and DHA from the diet partially replace the omega-6 fatty acids, especially AA, in the membranes of probably all cells, but especially in the membranes of platelets, erythrocytes, neutrophils, monocytes, and liver cells (reviewed in [3,32]). AA and EPA are the parent compounds for eicosanoid production. Because of the increased amounts of omega-6 in the Western diet, the eicosanoid metabolic products from AA, specifically prostaglandins, thromboxanes, leukotrienes, hydroxy fatty acids, and lipoxins, are formed in larger quantities than those derived from omega-3 fatty acids, specifically EPA [3]. The eicosanoids from AA are biologically active in very small quantities and, if they are formed in large amounts, they contribute to the formation of thrombus and atheromas; to allergic and inflammatory disorders, particularly in susceptible people; and to proliferation of cells [33]. Thus, a diet rich in omega-6 fatty acids shifts the physiological state to one that is proinflammatory, prothrombotic, and proaggregatory, with increases in blood viscosity, vasospasm, vasoconstriction and cell proliferation.
A balance existed between omega-6 and omega-3 fatty acids during the long evolutionary history of the genus Homo [34]. During evolution, omega-3 fatty acids were found in all foods consumed: particularly meat, fish, wild plants, nuts and berries [34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50]. Recent studies by Cordain et al. [51] on the composition of the meat of wild animals confirm the original observations of Crawford and Sinclair et al. [36,52]. However, rapid dietary changes over short periods of time as have occurred over the past 100–150 years is a totally new phenomenon in human evolution (Figure 1). A balance between the omega-6 and omega-3 fatty acids is a physiological state that is less inflammatory in terms of gene expression [53], prostaglandin and leukotriene metabolism, and interleukin-1 (IL-1) production [3].
Modern agriculture, by changing animal feeds as a result of its emphasis on production, has decreased the omega-3 fatty acid content in many foods: animal meats, eggs, and even fish [39,40,41,42]. Foods from edible wild plants contain a good balance of omega-6 and omega-3 fatty acids. Purslane, a wild plant, in comparison to spinach, red leaf lettuce, buttercrunch lettuce and mustard greens, has eight times more ALA than the cultivated plants [46]. Modern aquaculture produces fish that contain less omega-3 fatty acids than do fish grown naturally in the ocean, rivers and lakes [41]. The fatty acid composition of egg yolk from free-ranging chicken has an omega-6:omega-3 ratio of 1.3 whereas the United States Department of Agriculture (USDA) egg has a ratio of 19.9 [42]. By enriching the chicken feed with fishmeal or flaxseed, the ratio of omega-6:omega-3 decreased to 6.6 and 1.6 respectively.
Although diets differ in the various geographic areas [54], a number of investigators including Crawford [36], Cordain [51], Eaton [55] and Kupiers [56] have shown that during the Paleolithic period, the diets of humans included equal amounts of omega-6 and omega-3 fatty acids from both plants (LA + ALA) and from the fat of animals in the wild and fish (AA + EPA + DHA). Recent studies by Kuipers et al. [56] estimated macronutrient and fatty acid intakes from an East African Paleolithic diet in order to reconstruct multiple Paleolithic diets and thus estimate the ranges of nutrient intakes on which humans evolved. They found (range of medians in energy %) intakes of moderate-to-high protein (25%–29%), moderate-to-high fat (30%–39%) and moderate carbohydrates (39%–40%). Just as others have concluded previously, Kuipers et al. [56] stated, "compared with Western diets, Paleolithic diets contained consistently high protein and long-chain PUFA and lower LA". Guil-Guerrero J et al. [57] determined the fat composition of frozen mammoths (from 41,000 to 34,000 years BP), Bisons from early Holocene (8200–9300 years BP) and horses from middle Holocene (4600–4400 years BP), often consumed by Paleolithic/Neolithic hunters gatherers, and concluded, that "the animal fat contained suitable amounts of omega-3 and omega-6 fatty acids, possibly in quantities sufficient to meet today's dietary requirements for good health". The elucidation of sources of omega-3 fatty acids available for the humans who lived in the Paleolithic and Neolithic is highly relevant to ascertain the availability of nutrients at that time and to draw conclusions about healthy dietary habits for present-day humans. As in previous studies, the amount of ALA was higher than LA in the fat of the frozen specimens [58,59] (Table 3 and Table 4).
3. Effects of Omega-6 and Omega-3 Fatty Acids and their Ratio on Obesity
Experimental studies have suggested that omega-3 and omega-6 fatty acids may elicit divergent effects on body fat gain through mechanisms of adipogenesis [60], lipid homeostasis [61,62], brain-gut-adipose tissue axis [63], and systemic inflammation [64]. Metabolites of AA (20:4ω-6) play important roles in the terminal differentiation of pre-adipocyte to mature adipocyte [65]. This effect can be inhibited by omega-3 fatty acids at multiple steps [66,67,68,69]. Omega-6 fatty acids increase cellular triglyceride content by increasing membrane permeability [70], while omega-3 fatty acids reduce fat deposition in adipose tissues by suppressing lipogenic enzymes and increasing β-oxidation [71]. In addition, omega-6 and omega-3 fatty acids differentially modulate the brain-gut-adipose tissue axis [63] and the inflammatory properties of downstream eicosanoids, which ultimately affect pre-adipocyte differentiation and fat mass growth [72]. White adipocytes are storing energy in the form of triglycerides whereas brown adipocytes dissipate energy from triglycerides by producing heat (Table 5). In rodents and possibly in humans both types of fat cells participate in the total energy balance. By altering rates of adipocyte differentiation and proliferation, differences in fatty acid composition of dietary fats may also contribute to adipose tissue development, in particular with respect to the relative intake of omega-6 and omega-3 fatty acids. The omega-6/omega-3 ratio determines the availability of omega-6-AA within adipose tissue and thus the level of various prostaglandins derived from the cyclooxygenase-mediated pathways, which can be blocked by omega-3 fatty acids (Figure 2). Recent studies have shown that perinatal exposure of mice to a high omega-6 fatty acid diet (similar to Western diet) results in a progressive accumulation of body fat across generations, which is consistent with the fact that in humans, overweight and obesity have steadily increased in the last decades, and emerge earlier in life [12,73]. Furthermore, AA metabolites prostaglandins E2 and F2α have an inhibitory role in the browning process of white fat cells converted into energy-dissipating brown fat cells which are believed to play a role in controlling energy balance by lowering body weight [74,75,76,77,78,79,80,81,82] (Table 5).
High intake of omega-6 fatty acids during the perinatal period is associated with increased adiposity in the offspring. In human studies the level of AA in adipose tissue is associated with the BMI and overweight status of children. High omega-6/omega-3 fatty acids in umbilical cord red blood cell (RBC) membrane phospholipids was associated with high subscapular skin-fold thickness at 3 years of age [5].
Animal and human studies have shown that EPA and DHA supplementation may be protective against obesity, and may reduce weight gain in already obese animals and humans [83]. Specifically, studies demonstrated a reduction in visceral (epididymal and/or retroperitoneal) fat in rats fed high lipid diets that incorporate omega-3 PUFAs [75,78,79,84,85,86,87], and the effect was dose-dependent [85]. The reduction in visceral fat was associated with a decrease in adipocyte size [85,86] and number [87]. High fat diets rich in omega-6 fatty acids have been shown to increase the risk of leptin resistance, diabetes, and obesity in humans and rodents [76,88]. AA impairs hypothalamic leptin signaling and energy homeostasis in mice [77]. The inhibitory role of AA has been suggested in both basal and insulin-stimulated leptin expression and production [88].
3.1. The Fat-1 Transgenic Mouse Model
Many of the problems involving dietary animal studies can be overcome by the fat-1 transgenic mouse model that carries a Caenorhabditis elegans fat-1 gene encoding an omega-3 fatty acid desaturase. This enzyme can convert omega-6 to omega-3 fatty acids by adding a double bond at the omega-3 position [89]. Consequently, fat-1 not only increases the levels of omega-3 fatty acids but also concomitantly decreases omega-6 fatty acids as well as the omega-6/omega-3 ratio—a goal difficult to achieve through dietary means alone, yet important for health benefits. Although not fully equated to a dietary approach, the transgenic model produces the same types of omega-3 fatty acids as those obtained through diet [89].
Furthermore, the fat-1 model offers numerous advantages in the studies of the health benefits of omega-3 fatty acids, because the transgenic model allows elucidation of the mechanisms of actions of omega-3 fatty acids without the confounding issues associated with dietary approaches, such as dose, composition, and duration of treatment applied in different studies [16,90,91] (Table 2). The use of fat-1 mouse model avoids these concerns by feeding exactly the same diet to the transgenic and wild type (WT) mice. Because FAT-1 is an enzyme, the production of omega-3 fatty acids in mice is limited by the amount of available substrate: omega-6 fatty acids. The degree of increase in omega-3 fatty acids (3- to 4-fold) required to improve metabolic parameters in fat-1 transgenic mice has been shown to be achievable through dietary means in animals and humans [92]. Recently Li et al. [93] carried out a comprehensive study using the fat-1 model to better define how alterations in the tissue levels of omega-6 and omega-3 fatty acids affect energy balance, lipid and glucose metabolism, chronic inflammation, and the underlying molecular events (or mechanisms). Their results show that when challenged with high-fat diets, fat-1 mice strongly resisted obesity, diabetes, hypercholesterolemia, and hepatic steatosis. Endogenous elevation of omega-3 PUFAs and reduction of omega-6 PUFAs did not alter the amount of food intake but led to increased energy expenditure in the fat-1 mice. These metabolic phenotypes were accompanied by attenuation of the inflammatory state because tissue levels of prostaglandin E2, leukotriene B4, monocyte chemoattractant protein-1, and TNF-α were significantly decreased. The TNF-α-induced NF-κB signaling was almost completely abolished. Consistent with the reduction in chronic inflammation and a significant increase in peroxisome proliferator-activated receptor-γ activity in the fat-1 liver tissue, hepatic insulin signaling was sharply elevated. The activities of prolipogenic regulators, such as liver X receptor, stearoylCoA desaturase-1, and sterol regulatory element binding protein-1 were sharply decreased, whereas the activity of peroxisome proliferator-activated receptor-α, a nuclear receptor that facilitates lipid β-oxidation, was markedly increased [93]. Thus, endogenous conversion of omega-6 to omega-3 PUFAs via fat-1 strongly protects against obesity, diabetes, inflammation, and dyslipidemia and may represent a novel therapeutic modality to treat these prevalent disorders.
3.2. Human Studies
Randomized controlled trials in humans examining the relationship between omega-3 supplementation and body composition have produced conflicting results due to many factors summarized in Table 2 [19,83]. This may be due to differences in study design, dosage, not taking into consideration the omega-6/omega-3 ratio of the background diet, timing, and duration of omega-3 PUFA administration, use of other supplements in addition to omega-3 PUFA, and demographics of the study population. Furthermore, in many studies the determination of omega-6/omega-3 fatty acids was based on food frequency questionnaires, which are not as accurate as direct measurements of fatty acids in RBC membrane phospholipids. Several studies have provided supporting evidence for a role of omega-3 PUFAs in body composition [94], weight reduction [95], less hunger and more fullness [96]. These findings support a potential role for omega-3 in appetite regulation in humans. Some intervention studies showed that omega-3 fatty acid supplementation reduced body weight and obesity in lean [14], overweight [95,97] and obese [98] individuals. Couet et al. [14] noted a 22% increase in basal lipid oxidation with 6 grams of fish oil for 3 weeks. Omega-3 fatty acids are long term metabolic fuel partitioners with greater partitioning towards β-oxidation in men than in women.
Omega-6 and omega-3 red blood cell membrane phospholipid determinations represent biomarkers of dietary intake plus endogenous metabolism and represent the most accurate way to carry out preventive studies and clinical intervention studies to evaluate their role in weight gain and obesity [99]. Wang et al. [100] conducted a prospective analysis to examine the association of baseline red blood cell membrane phospholipids of omega-3 fatty acids, omega-6 fatty acids, omega-6/omega-3 ratio and trans fatty acids with the longitudinal changes in body weight and the risk of becoming overweight or obese during a mean of 10.4 years follow up in the NIH Women's Health Initiative Study. The results of this prospective study showed that baseline red blood cell membrane phospholipids cis omega-3 fatty acids is inversely associated, and cis omega-6 fatty acids are positively associated, with longitudinal weight gain in initially normal weight healthy women. This is the first study to prospectively examine omega-3 and omega-6 fatty acids in red blood cell membrane phospholipids in relation to weight gain and the risk of becoming overweight or obese. After multivariable adjustment, significant positive associations with weight gain were found only for dihomo-γ-linolenic acid (DGLA), LA, and Gamma-linolenic acid (GLA) among omega-6 fatty acids and trans 18:1 among trans fatty acids; while inverse associations were found with EPA among omega-3 fatty acids. The authors state that, "the variations by individual fatty acids may be due to unknown and uncontrolled factors involved in the conversion and metabolism of each fatty acid, and should be interpreted cautiously given the multiple comparisons. This study included only women who had normal BMI at baseline to minimize potential confounding and address the risk of becoming overweight or obese". To further evaluate the impact of baseline BMI on the results, Wang et al. [100] stratified analyses by baseline BMI levels (18.5–≤23, 23–≤25 kg/m2) and also included women who were already overweight or obese at baseline (baseline BMI ≥ 25 kg/m2) in sensitivity analyses. Similar patterns of associations were found in these additional analyses. In conclusion, this prospective study provided strong suggestive evidence that omega-3 fatty acids in RBC membrane phospholipids are inversely associated, while cis omega-6 fatty acids, omega-6/omega-3 ratio, and trans fatty acids are positively associated, with longitudinal weight gain.
4. Genetics: The Fat Mass and Obesity-Associated Gene
Genome-Wide Association Studies (GWAS) have identified more than 90 loci that contain genetic variants associated with obesity. Many of these variants are in intronic regions. The strongest genetic association with risk to polygenic obesity are single-nucleotide variants (SNV) in intron 1 and 2 of the FTO (fat mass and obesity associated) gene. There are 89 SNVs in FTO intron 1 and 2. Deciphering how these variants regulate gene expression has been difficult. Recently Claussnitzer et al. [101] reported a strategy and defined the causal SNV and the mechanisms of function in preadipocytes. The authors provide evidence for the rs 1421085 T to C SNV to result in a cellular phenotype consistent with obesity in primary human adipocytes, including decreased mitochondrial energy generation and increased triglyceride accumulation.
Their study provided evidence that the risk allele rs 1411085 T to C SNV resulted in increased expression of IRX3 and IRX5 genes in pre-adipocytes, which shifted the development of these cells toward the "white program" and increased lipid storage, whereas knockdown of IRX3 and IRX5 genes restored thermogenesis in adipocytes from persons at high risk for obesity. Thus, the risk allele functioned similarly to AA metabolites, PGI2 and PGF2a, increasing proliferation of white adipose tissue and decreasing its browning respectively, whereas the knockdown of IRX3 and IRX5 genes functioned similarly to omega-3 fatty acid metabolites increasing the browning of the adipose tissue, mitochondrial biogenesis and thermogenesis. The arachidonic acid metabolites PGI2 and PGF2a lead to increases in white adipose tissue and decreases its browning respectively. Human studies have shown a direct relationship between plasma arachidonic acid levels and infant body weight, as well as between AA levels in adipose tissue lipids and BMI in children in Cyprus and Crete [102,103]. AA directly inhibits UCPI gene expression. Considering the high omega-6/omega-3 fatty acid ratio of Western diets and the role of AA in adipose cell differentiation, proliferation, and decreasing browning of white adipose tissue, further research should include studies on the effects of omega-3 fatty acids in blocking the effects of the risk allele (rs 1421085), which appears to be responsible for the association between the first intron of FTO gene and obesity in humans.
5. Omega-6/Omega-3 Fatty Acid Ratio: Endocannabinoid System
A diet high in the omega-6/omega-3 ratio causes an increase in the endocannabinoid signaling and related mediators, which lead to an increased inflammatory state, energy homeostasis, and mood. In animal experiments a high omega-6 acid intake leads to decreased insulin sensitivity in muscle and promotes fat accumulation in adipose tissue. Nutritional approaches with dietary omega-3 fatty acids reverse the dysregulation of this system, improve insulin sensitivity and control body fat.
Endocannabinoids are lipids, derived from the omega-6 AA. Their concentrations are regulated by (1) dietary intake of omega-6 and omega-3 fatty acids; and (2) by the activity of biosynthetic and catabolic enzymes involved in the endocannabinoid pathway, which is an important player in regulation of appetite and metabolism [81,104]. The endocannabinoid system is involved in regulation of energy balance and sustained hyperactivity of the endocannabinoid system contributes to obesity [81,82]. AA is the precursor of 2-arachidonoylglycerol (2-AG) and anandamide (AEA). Increasing the precursor pool of AA causes excessive endocannabinoid signaling leading to weight gain and a metabolic profile associated with obesity. Endocannabinoids activate endogenous cannabinoid CB1 and CB2 receptors in the brain, liver, adipose tissue, and the gastrointestinal tract [105]. Activation of CB1 receptors in the hypothalamus leads to increased appetite and food intake [82]. In mouse experiments endocannabinoids selectively enhance sweet taste, which in the current highly palatable food supply stimulate food intake [106]. The endocannabinoid system functions in concert with other systems regulating food intake and energy balance, and is regulated by leptin, insulin, ghrelin, cholecystokinin, and other signals. Targeting the endocannabinoid system has been a strategy for weight loss. Randomized controlled clinical trials in overweight or obese humans showed that CB1 receptor antagonists such as rimonabant led to significant weight loss after one year of treatment [107]. However the drug was withdrawn from the market due to severe side effects that led to increased risk of anxiety, depression, and suicide [108].
Alvheim et al. [80] carried out an experiment in mice at six weeks of age, in which increasing the linoleic acid in the diet led to increases in AA in red blood cell membrane phospholipids, elevated 2-AG and AEA in liver, elevated plasma-leptin and resulted in larger adipocytes and more macrophage infiltration in adipose tissue. It was also noted that a higher linoleic acid increased feed efficacy and caused greater weight gain than isocaloric diets containing less LA. Increasing the dietary LA from 1% to 8% of energy increased liver endocannabinoid levels, which increased the risk of developing obesity, even in a low fat diet. Mice chronically deficient in omega-3 PUFA have significantly lower concentrations of DHA in brain phospholipids, and higher 2-AG (derived from AA) compared to mice with sufficient omega-3 PUFA in their diet [82]. Furthermore, omega-3 PUFA supplementation of mice with 10% weight DHA-rich fish oil for 4 weeks led to higher brain DHA levels compared to mice on a low omega-3 PUFA diet, and led to a significant decrease in brain 2-AG and brain AA. This nutritional approach with dietary omega-3 PUFA, reversed the dysregulation of the cannabinoid system, improved insulin sensitivity and decreased central body fat.
6. Conclusions and Recommendations
- Human beings evolved on a diet that was balanced in the omega-6 and omega-3 essential fatty acids.
- A high omega-6 fatty acid intake and a high omega-6/omega-3 ratio are associated with weight gain in both animal and human studies, whereas a high omega-3 fatty acid intake decreases the risk for weight gain. Lowering the LA/ALA ratio in animals prevents overweight and obesity.
- Omega-6/omega-3 fatty acids compete for their biosynthetic enzymes and because they have distinct physiological and metabolic properties, their balanced omega-6/omega-3 ratio is a critical factor for health throughout the life cycle.
- Adipose tissue is the main peripheral target organ handling fatty acids, and AA is required for adipocyte differentiation (adipogenesis). The increased LA and AA content of foods has been accompanied by a significant increase in the AA/EPA + DHA ratio within adipose tissue, leading to increased production in AA metabolites, PGI2 which stimulates white adipogenesis and PGF2α which inhibits the browning process, whereas increased consumption of EPA and DHA leads to adipose tissue homeostasis through adipose tissue loss and increased mitochondrial biogenesis.
- High omega-6 fatty acid intake leads to hyperactivity of endocannabinoid system, whereas omega-3 fatty acids lead to normal homeostasis (decrease hyperactivity).
- High omega-6 fatty acids increase leptin resistance and insulin resistance, whereas omega-3 fatty acids lead to homeostasis and weight loss.
- Because a high omega-6/omega-3 ratio is associated with overweight/obesity, whereas a balanced ratio decreases obesity and weight gain, it is essential that every effort is made to decrease the omega-6 fatty acids in the diet, while increasing the omega-3 fatty acid intake. This can be accomplished by (1) changing dietary vegetable oils high in omega-6 fatty acids (corn oil, sunflower, safflower, cottonseed, and soybean oils) to oils high in omega-3s (flax, perilla, chia, rapeseed), and high in monounsaturated oils such as olive oil, macadamia nut oil, hazelnut oil, or the new high monounsaturated sunflower oil; and (2) increasing fish intake to 2–3 times per week, while decreasing meat intake.
- In clinical investigations and intervention trials it is essential that the background diet is precisely defined in terms of the omega-6 and omega-3 fatty acid content. Because the final concentrations of omega-6 and omega-3 fatty acids are determined by both dietary intake and endogenous metabolism, it is essential that in all clinical investigations and intervention trials the omega-6 and omega-3 fatty acids are precisely determined in the red blood cell membrane phospholipids. In severe obesity drugs and bariatric surgery have been part of treatment.
- The risk allele rs 1421085 T to C SNV in intron 1 and 2 in the FTO gene functioned similarly to AA metabolites, PGI2 and PGF2a increasing proliferation of white adipose tissue and decreasing its browning respectively, whereas the knockdown of IRX3 and IRX5 genes functioned similarly to omega-3 fatty acid metabolites increasing the browning of white adipose tissue, mitochondrial biogenesis, and thermogenesis. Therefore, further research should include studies on the effects of omega-3 fatty acids in blocking the effects of the risk allele (rs 1421085), which appears to be responsible for the association between the first intron of FTO gene and obesity in humans.
- In the future studies on genetic variants from GWAS will provide opportunities to precisely treat and prevent obesity by both nutritional and pharmaceutical interventions.
Obesity is a preventable disease that can be treated through proper diet and exercise. A balanced omega-6/omega-3 ratio 1–2/1 is one of the most important dietary factors in the prevention of obesity, along with physical activity. A lower omega-6/omega-3 ratio should be considered in the management of obesity.
I have not received any source of funding for this article.
Conflicts of Interest
The author declares no conflict of interest.
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- Artmann, A.; Petersen, G.; Hellgren, L.; Boberg, J.; Skonberg, C.; Nellemann, C.; Hansen, S.H.; Hansen, H.S. Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine. Biochim. Biophys. Acta 2008, 1781, 200–212. [Google Scholar] [CrossRef] [PubMed]
- Yoshida, R.; Ohkuri, T.; Jyotaki, M.; Yasuo, T.; Horio, N.; Yasumatsu, K.; Sanematsu, K.; Shigemura, N.; Yamamoto, T.; Margolskee, R.F.; et al. Endocannabinoids selectively enhance sweet taste. Proc. Natl. Acad. Sci. USA 2010, 107, 935–939. [Google Scholar] [CrossRef] [PubMed]
- Van Gaal, L.; Pi-Sunyer, X.; Despres, J.P.; McCarthy, C.; Scheen, A. Efficacy and safety of rimonabant for improvement of multiple cardiometabolic risk factors in overweight/obese patients: Pooled 1-year data from the Rimonabant in Obesity (RIO) program. Diabetes Care 2008, 31, S229–S240. [Google Scholar] [CrossRef] [PubMed]
- Christensen, R.; Kristensen, P.K.; Bartels, E.M.; Bliddal, H.; Astrup, A. Efficacy and safety of the weight-loss drug rimonabant: a meta-analysis of randomised trials. Lancet 2007, 370, 1706–1713. [Google Scholar] [CrossRef]
Figure 1. Hypothetical scheme of fat, fatty acid (ω6, ω3, trans, and total) intake (as percent of calories from fat). Data were extrapolated from cross-sectional analyses of contemporary hunter-gatherer populations and from longitudinal observations and their putative changes during the preceding 100 years (Modified from [3]).
Figure 2. Oxidative metabolism of arachidonic acid (AA) and eicosapentaenoic acid by the cy-clooxygenase and 5-lipoxygenase pathways. 5-HPETE denotes the 5 hydroperoxyeicosatetranoic acid and 5-HPEPE denotes the 5-hydroxyeicosapentaenoic acid [3].
Figure 3. Desaturation and elongation of ω-3 and ω-6 fatty acids by the enzymes fatty acid de-saturases FADS2 (D6) and FADS1 (D5).
Table 1. Effects of Ingestion of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from Fish or Fish Oil. Modified from [3].
Table 2. Factors that affect outcomes in Obesity studies leading to conflicting results in clinical intervention trials (Modified from Reference [19]).
|- Determination of the composition of the background diet in terms of omega-6 and omega-3 fatty acids and inflammatory markers i.e., US, UK and Northern European countries have the highest amount of LA + AA in their diets, which competes with omega-3 PUFAs; they also have the lowest amount of vegetable and fruit intake, which are needed for optimal absorption of omega-3 PUFA from supplements
|- Background inflammation
|- Some studies are using fish and others omega-3 supplements; studies show that a continuous daily intake of omega-3 supplements leads to higher concentrations in the blood than eating fish two times/week
|- Variation in the dose of omega-3 fatty acids
|- Variation in the number of subjects
|- Variation in the severity of disease
|- Variation in the pharmacologic treatment
|- Genetic variants predisposing to Obesity
|- Dietary intake by means of questionnaires instead of actual measurements of omega-3 PUFAs in the red blood cell membrane phospholipids or plasma is a major problem that leads to conflicting results
|- Length of intervention
|- Genetic variants in the metabolism of omega-6 and omega-3 fatty acids
Table 3. Estimated Omega-3 and Omega-6 Fatty Acid intake in the Late Paleolithic Period (g/day) a,b,c.
|AA (ω6)
|EPA (ω3)
|DTA (ω6)
|DPA (ω3)
|DHA (ω3)
|Ratios of ω6/ω3
|Total ω6/ω3
|0.79 b
a Data from Eaton et al. [58]; b Assuming an energy intake of 35:65 of animal: plant sources; c LA, linoleic acid; ALA, linolenic acid; AA, arachidonic acid; EPA, eicosapentaenoic acid; DTA, docosatetranoic acid; DPA, docosapentaenoic acid; DHA, docosahexaenoic acid.
|Greece prior to 1960
|Current Japan
|Current India, rural
|Current UK and northern Europe
|Current US
|Current India, urban
|Adipogenesis (Pre-adipocyte-Adipocyte)
|High AA via the PI2 receptor activates the cAMP protein kinase A, signaling pathway leads to proliferation and differentiation of WAT, prevention of its browning through inhibition of PPARy target genes including UCPI, decrease mitochondrial biogenesis [74], increasing triglycerides [73], insulin resistance, leptin resistance, decreased adiponectin levels, decreased fatty acid oxidation and hepatic steatosis [4].
|High EPA and DHA partially inhibit cAMP signaling pathways triggered by AA at levels upstream of PKA [71] block COX-2 metabolites PGI2 and PGEF2a that stimulate white adipogenesis and inhibit the browning process respectively, prevent increased triglycerides and adipose tissue proliferation through UCP-I and PPARy activation, increased mitochondrial biogenesis, increased fatty acid oxidation, and apoptosis [71,75].
|AA metabolites prostaglandin 2 thromboxane 2 and leukotriene 4 are prothrombotic and proinflammatory leading to increased production of IL-1, IL-6, NFKB and TNF and inflammation [1,64].
|High dietary intake of EPA and DHA blocks the metabolites of AA and prevents inflammation, which is the hallmark of obesity [1,64,67].
|Insulin Resistance Leptin Resistance Adiponectin
|AA leads to insulin resistance, leptin resistance, lower adiponectin and hepatic steatosis. AA blunts PI3-Akt pathway leading to leptin resistance in the brain and deregulation of food intake [19,76,77].
|EPA and DHA regulate glucose utilization, insulin sensitivity (Akt phosphorylation) in part mediated by PPARy and AMPK activation [19]. EPA and DHA regulate the secretion of adipokines involved in energy homeostasis and intermediate metabolism and in glucose and lipid metabolism. DHA restores insulin sensitivity in skeletal muscle by preventing lipotoxicity and inflammation [78,79].
|AA increases the concentration of (2-AG) and (AEA) leading to excessive endocannabinoid signaling, and dysregulation of the cannabinoid system, weight gain, larger adipocytes and more macrophages in adipose tissue [80], inflammation and a metabolic profile associated with obesity [81,82].
|EPA and DHA decrease 2-AG and AA in the brain while increasing DHA, decreasing the dysregulation of the cannabinoid system, improving insulin sensitivity and decreasing central body fat.
© 2016 by the author; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).


text:
In case you hadn't noticed, I am a fan of music as well as the sea. My tastes do tend to run traditional and older. I may have frozen on '70s and '80s rock and I was one of the tribe who followed the Dead from coast to coast for a wonderful, rather fuzzy year.
Thanks, as always to my wonderful betas, Breathesgirl and Ms Buffy.
And thank you to Sephrenia who crafted the banner for this story. I tend to work from outlines and 'keep to the code,' as it were, but when I saw the images Seph created, I had to incorporate them into the story. Still a few chapters to go, but you'll see what I mean.
Happy Tuesday

subset: commoncrawl


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text: Excited as we are about the new Student Activities and Events Center? You've come to the right place! Check back weekly for progress pictures of the site and watch the new building come to life. We can't wait! If you want to see all the pictures from the project, visit our Flickr page. You can also check out the live camera at the site any time.


text:
Kettel one KitchenWed Nov 14th 2018 at 19:00
Panama, 5incoPanama https://www.myguidepanama.com/events/ketel-one-kitchen VISIT WEBSITE
Event Details
5inco Panama & Ketel One Vodka, invites you to participate in the "Mixology Workshop", which will take place on Wednesday, November 14 at 7:00 p.m. In this opportunity you will learn from the Global Brand Ambassador Paulo Figueiredo the most natural and fresh preparations in the most traditional way.
Mythology or cocktail making is the art of mixing drinks in a delicate balance where everything counts, from the selection of the ingredients, to the way of uniting them, the balances and the contrasts.
This workshop will provide all the tools to learn about the basis of a cocktail, where they come from, what they are made of, analyzing flavors, aromas, textures, colors, densities, levels of alcoholic volume, combining balance and harmony in their content.
For more information and to reserve your quota you must contact the number: 203-4574
My Guide website?


text:
|Ruby Dee (1924 - )
Mrs. Ossie Davis (widowed)
|The Stand (1994) [Mother Abigail Freemantle]: Dies of old age/natural causes, with several of her followers by her bedside. (She's made up to look much older than she actually was at the time.)
Captive Heart: The James Mink Story (1996) [Indigo]: Reportedly beaten and tortured to death. (Thanks to Michael)


text:
And some insight I miss. Let's start with the wizemen that I miss:
New Yorker in DC: Where've ye gone fella?
Hidden Unities: Via his meeting with Dan, I suspect Ed's on something of an American sojourn and good on him for that.
Now the wizened:
Dreaming 5GW: Arherring's latest endeavor and the commentary that follows. Nuts and bolts, fellows, nuts and bolts.
Got Critt: This guy's an enigma, point blank. Very much reminiscent of a recently deceased friend.
Olly's Onions: Lord Humungus is a frightening sort, isn't he? We, apparently, do need another hero...
Coming Anarchy: Chirol unveils a discussion regarding the 12/10 decision that will propose an independent Kosovo.
Good stuff
7 years ago


text:
America Addicted
The new face of this drug crisis will shock you. PBS NewsHour's Hari Sreenivasan join us with a report.
Title: America Addicted
Type: Segment
Subject(s): Opioids Crisis
Public Broadcasting Station or Institution: WLIW | MetroFocus
Original Broadcast/Publish Date: 10/12/2017
Runtime: 00:06:38
Rights Information:
Sensitive Material:
Special Instructions: N/A
File Clean of Graphics: No
Language: English


text:
Blue Lotus Sanctuary
Blue Lotus Sanctuary and Community Village
Imagine …
✨ A peaceful community in the beauty of nature, where we serve the earth that is under our holy protection ✨
✨ The opportunity to immerse in deep wisdom teachings, practices, and integration on the soul level with other like-minded people ✨
✨ A judgment-free space where unique, individual expression and authentic presence is woven into the fabric of everyday life ✨
✨ A sacred cauldron of inspiration, protection, love and unified consciousness ✨
We are currently raising funds to acquire the land where this vision can be anchored: We want to create a spiritual community based on earth stewardship which embodies the values and principles of the Temple of Sacred Arts, which you can read more about here.
How will the community work?
✨The community will be run along permaculture principles. ✨
✨ We aim to be fully self-sustaining within the first 3 years in terms of food and energy. ✨
✨ We will start with the permaculture aspect and then build the school and the accommodation. ✨
✨ We will use natural material for building purposes and accommodate traditional practices in as many aspects as possible. ✨
✨ We will stay fully off grid. ✨
✨ We will create orchards, a vegetable garden and a medicinal herb garden and will have both an outdoor and indoor kitchen. ✨
On a day-to-day basis, the community will be run mostly by trainee priestesses who live on site or nearby.
We will welcome volunteers and students to have immersive experiences in the community, coming to learn about permaculture, sustainable living and wisdom teachings. We will not charge for stays but as the project develops we may offer experiences, tools and products for sale as part of the experience.
What will people get out of visiting our community?
The opportunity to work and live within an earth-based, Goddess-focused community
A return to nature
Experiencing a sense of freedom and creative expression that is extremely rare in our society
Training in the ancient arts and traditional Earth Priestessing. This will be grounded in real-life experience rather than just theory.
Where we are now
We are currently at the first stage of fundraising, where we need to acquire the land. We are looking for between 3.5 – 5 acres with a water source, a bit of woodland and either an old farmhouse or a barn we can convert.
We are looking at the areas of Somerset and Devon and also the Republic of Ireland. Auctioned farms would be the best option.
How you can become part of our exciting vision
By becoming a donator, you will be supporting us to …
… Create a community where the depth of our communion with the earth receives ample time, space and creativity, restoring us to harmony with ourselves, each other and our Mother Gaia.
… Give vital education opportunities in the skills of sustainable living. This is increasingly urgent in these times of environmental crisis.
… Bring the values of earth-honouring and feminine, ancient spiritual paths back into the world, so that more people can experience a deeper connection to their spirits and themselves.
… Seed an exciting development in community living, where we can learn, grow and expand together, each giving our unique gifts to co-create something greater than we could alone.
Any and every amount is beyond a blessing and greatly appreciated.
The Benefits of Donating to our project
Supporters who donate £ 50 (single membership) or £ 75 (double membership) will become a Friend of Blue Lotus Sanctuary. The benefits include an invitation to our Solstice Ceremony event twice a year, an exclusive monthly newsletter, and, of course, the satisfaction of knowing you're helping to birth this life-enhancing, earth-protecting project into the world.
If you choose to donate £ 500 or more, you will receive:
- A 30 % discount on all courses and workshops offered by the Temple.
- Private use of the facilities available on the land on selected days.
- Plus all the same privileges as Friends.
Generous donations of £ 1 000 – £ 10 000 will give you Guardian status. This involves receiving:
- A share of our produce and use of our Sacred Space.
- Invitations to our Annual Guardians Dinner and Embodiment Evening.
- Monthly Report on our progress and projects.
- Plus the same privileges as Pioneers.
Let's raise a community of wisdom, insight and co-creation that sustains our earth for generations to come. Please share widely among your networks. With deep and humble gratitude for your love, support and generosity.
or visit our Go Fund Me
Visit our community page to find out more about our offerings and devotional work.


text:
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|Glen Arm
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Flightglobal.com has a new look for the new year. The world's best-read aviation news website is putting the focus firmly back on breaking news, analysis, comment, features and visual content, with redesigned channels that make it easier to see the latest and trending stories, across sectors such as Airlines, Manufacturing, Defence, and Business Aviation. We have also introduced larger images, easier-to-read lists of headlines, and a cleaner, less cluttered design.
We have simplified the navigation, so it is not only quicker to locate the industry news you need, but also dozens of job vacancies and careers advice, as well as information on our global programme of conferences and events, special promotions, and our ever-popular searchable archive that allows you to read pages of the world's oldest aviation magazine, going back to the birth of the industry in 1909.
We have listened to your feedback that told us you wanted a site that reflected the changing dynamics of the global industry, with prominence for the stories being reported by our team of more than 20 journalists around the world, and that was easier to find your way around.
As well as being part of the industry's leading data solutions provider, flightglobal.com builds on the heritage, reputation, and expertise of our two magazine brands, the weekly Flight International and Airline Business monthly, in addition to our Flight Daily News air show newspapers – but with all our content in one place, and now easier to find and peruse. Watch out for further enhancements to the site during 2019.
Source: Flight Daily News


text:
We'll end the storyline here... I know the mood's darkened a little, but I'll lighten things up next week.
Comic transcript
TRANSCRIPTION COURTESY OF JOSEPH HOUK - (PW, greeting CW as she arrives home – and seeing that she's been crying) "Cassie, you alright? What happened?" (CW) "I must've cried the whole trip back home. Philip, I just fucked EVERYTHING up." (PW, hugging her) "Nothing doing, huh? I'm so sorry, dear." (CW) "It's okay. I need to just let go of this. As much as I hate it, Mom's a lost cause now. [looking up at her] I'm just gonna end up wrecking myself emotionally if I try and do anything else about this shit. And I don't want that. You don't want that. So at this point, whatever happens, happens." (PW) "Maybe you can get the video of the wedding and then go back and show it to your mom just before she dies?" (CW) "You know, I just love your fourth-dimensional thinking sometimes."


text:
The Accountancy Cloud have been shortlisted for the British Accountancy Awards for Independent Firm of the Year 2018. This was an award that we won last year.
It is great to share this news with our clients, partners, suppliers, accelerators and friends, we couldn't do any of this without your collaboration and support.
If you would like to speak to us about our services please do not hesitate to contact us .


text:
Dude, life sucks.
Okay, so, I moved into a new house, right? My parents are separated now. No, I am not sad and please stop telling me I should be sad because I'm happy. I'm more calm and less angry now.
Nonetheless, I moved. I have a new bedroom, bathroom, kitchen.
It's my fourteenth house.
I had this hope during summer that I would leave South Korea, that I would go to Paraguay and live in an apartment my father is buying. I'd have my own room and I would get to decorate it. Heck, I actually used Pinterest for once and made a board of all the themes and things I'd want in my room.
Now that hope is gone. Due to stuff in life, there's no point in that board anymore because I obviously won't be getting my own house until I'm an adult.
That's another thing, I'm scared of being an adult because what if I have that urge to pack up my bags every three years and move somewhere new? That's gonna cost a TON of money and from what I've seen with my parents, that doesn't seem very fun. Not to mention the amount of times they thought they'd own this house forever but only lived in in for two or three years. Bye, pink bedroom. Blue and purple bedroom. White bedroom.
And that's another thing. You know how I'm fourteen and I worry about boyfriends and stuff like that? Yay! I don't have to worry about losing my virginity much less having a boyfriend while I'm in Korea 'cause I'm crazy! Wooo!
Not what I meant to say but what if I decide to date? Is my boyfriend really gonna move around every two or three years? How long will he be able to handle that? And I don't want to date a TCK because I don't want to move every two or three years, I want a HOUSE. I want FRIENDS.
Do not worry, dear reader! I have a friend in Korea! He's in the grade above me and we only have Spanish class together.
But, I'm selfish and I love being social so I kind of want more friends, ya know? Friends I can talk to in real life. But I love my friends from the States so much and they're amazing yeah.
Anyway, on with a rant about me because I'm egotistical and want to feel sorry for myself.
Did you know I'm the only Western kid in the high school? Okay, there are probably Western kids but I'm the only "Wester" looking one. They can at least fit in the uniforms. My Western body doesn't fit well in them.
And I want to be a Western teenager, ya know, go to parties on the weekends? Have sleepovers?
If there are parties, I haven't heard of them or am invited. And sleepovers? I've tried with the previous friends I've had but as one explained to me, in their culture, they don't do sleepovers at this age.
Goodbye stupid ideas like drinking with friends, doing drugs, being rebellious. I just get to sit in my room and either study, watch YouTube, or a read a book. I don't have any hobbies 'cause I gave up on life. No, I'm not suicidal, stop it. You're gonna take it the wrong way but that's not it. I just don't see the point in life. What good does this species do, huh? And none of the adults I see seem very happy so what about me?
Oh and the haunting fact that I'm a TCK and lose my friends every two to three years.
Yeah, what a great life I live.
But, ya know, "be strong, that's what life's like"
So then if this is life, WHY, WHY WOULD I WANT TO BE ALIVE?
Once again, I am NOT suicidal, I'm just questioning things.
That's another thing, all the kids my age are either oblivious to life, oblivious and depressed, or depressed.
What kind of generation is this? What does that say about our society? It can't be entirely our faults that we're depressed, can it?
Anyway, I'm fourteen so what could I know? I'm just a dumb brunette who doesn't understand anything about the world, right? I couldn't possibly have meaningful conversations because I don't think that deeply.
So yeah, I've given up on life. I have being a TCK, it sucks.
You have no roots, you leave your friends, you're lonely.
As an ambivert, I don't really know how an introvert would feel about this but I think as human we all crave to be around humans once in a while and THAT IS NOT WHAT YOU GET WHEN YOU LIVE MY SPECIFIC
Let me say that word again
Other TCKs might have wonderful lives! Yay! I'm so happy for you! Congrats!
I want a room. I want my own room to hide in. A room that scream my personality. I want to paint the walls and have decorations hanging from the walls.
I want to go to the mall every once in a while or go somewhere and not just go to school the home
School then home
School then home
"PUT YOURSELF OUT THERE MORE!" I hear ya saying!
Number one, last year I did.
Number two, could you please let me, a teeneger, feel sorry for myself.
I do have friends outside of my school that I can talk to
I'm kind of trying to find people IN my school that don't mind my personality.
Shhh, I know, "go talk to the people you can talk to and enjoy their company"
And have other friends
Remember, they are in different schools
"Well at least you have friends!"
That I see every couple months, yes
Yay for those friends.
And after writing this all out, I don't feel like complaining about the friends I have because I have them and I'm done feeling sorry for myself
But diid I mention that I want a house? Did I say that yet?
I know what I said last year "YAY FOR BEING A TCK! WHAT A WONDERFUL LIFE"
Let me fix that to my pity-party-self now
"You need to talk to someone about this"
Yeah, I am.
But this is a blog for world nomads and TCKs, right? And I'm supposed to talk to you about my life as a TCK, right?
So, here you go, this is how I feel right now. Nothing edited out, nothing censored. It's how I feel.


text:
Rolling Store Man
NOTE:√ǬÝ√Ç¬Ý √ǬÝDue to the depression and then W.W.II, cars were rare amongst the country folk where I grew up.√Ç¬Ý Going to the store required arranging transport in advance, or walking, or riding your plow horse.
So enterprising merchants got themselves old vans or buses, installed shelves, ice chests, stocked them with merchandise and voila' – the Rolling Store was created.
Day to day life in the woods seldom varied.√Ç¬Ý If we had visitors, it was usually some one needing Daddy'Äôs help either to take them to the hospital in Clanton for emergencies such as broken bones, getting gored by a bull and once a neighbor hemorrhaging with TB, or to borrow the money to pay for those medical bills.√Ç¬Ý Daddy gave it to them even knowing he'Äôd probably never get it back.
So when Bernerd and I saw a bus-like vehicle creak down our long drive and pull-up under our massive oak tree – well, that was exciting, cause Rolling Store Man had arrived.
Rolling Stores didn'Äôt adhere to a schedule, so Mama couldn'Äôt plan a head and have money on hand, but that wasn'Äôt a problem.√Ç¬Ý What with her being known as The Praying Woman, her produce was trusted and sought after.√Ç¬Ý Rolling Store Man, gladly traded for Mama'Äôs chickens, eggs, butter and canned blackberries and huckleberries and their jams.
When he pulled up and parked, first he and Mama would determine what kind of chickens his customers wanted, whether pullets, baking hens, a yard rooster, or fryers and send Bernerd and me to round them up.√Ç¬Ý She took care of the more delicate and breakable merchandise.
Rolling Store Man weighed the chickens, stuffed them in cages he kept in the back of the bus, then he and Mama got down to the serious business of haggling till the value of everything was struck at that time Mama would buy.
She let me stand inside the Rolling Store beside her, where I could feast my eyes on all those fascinating items Rolling Store Man had on his shelves: Phials of first aid supplies – merthiolate, mercurochrome – rolls of adhesive tape and gauze, menthol gum for making lineament, boric acid for making sore eye solution and beautiful blue stone crystals used to cure ground itch on horses hooves.
There were tins marked with scull and crossbones, which√Ç¬Ý I longed to open just to see what poisons looked like, what color they'Äôd be, and if they would explode if I mixed them together.√Ç¬Ý I'Äôd ask questions about explosive probabilities and Bernerd, being four years older than me, would try to drag me out of the store, but I'Äôd hold on the door frame thwarting his efforts.
There were the spools of thread and packets of needles to tempt my hands, but Mama was strict.√Ç¬Ý I was never allowed to touch anything less Rolling Store Man think I might steal.
That was OK, for I knew Mama would buy us some candy, which was featured prominently on the shelves by the entrance 'Äì boxes of the luscious tasting, to Bernerd and me, rarity.√Ç¬Ý I loved the penny candy.√Ç¬Ý It sat in those boxes just sparkling at me.√Ç¬Ý All those blues, yellows, reds and greens looked like gemstones.
When Mama completed her purchases, and Rolling Store Man trundled back down the drive, she'd hand us each a candy bar and a nickel's worth of penny candy.
Bernerd and I would sit on the big roots under the Oak to eat our candy bar, lick our penny suckers, knowing that we were also in for a treat at√ǬÝsupper 'Äì hoop cheese and bologna, sliced from a stalk, served on lite bread.
Wow!√Ç¬Ý Life was goo-ood that day.
May 29, 2010
· Carolyn · 3 Comments
Tags: bartering, country life, rolling store · Posted in: country life
3 Responses
Sue - May 30, 2010
Mama was known as the Praying Woman?
P. S. I remember penny candy too!
Melanie - May 31, 2010
Oh, do I enjoy your stories. I can picture you taking it all in when the Rolling Store Man came to your house. It's the little things in life we should treasure, and you certainly did. More children should be like that today.
Kat - June 2, 2010
Very sweet. It's very nice to reminisce about simpler times. I wonder if you knew how lucky you were. Love, Kat