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Currently, 1 in 3 people have an adiposity-based chronic disease (ABCD), a situation that in recent decades has been on the rise. The systemic oxidative stress characteristic of ABCD is a complex and systemic state that derives from the deregulation of the musculoskeletal system and the loss of cellular antioxidant capacity. In the present review, we analyze the mechanisms of antioxidant bioactive compounds that, in clinical evidence, have shown a potential effect on the reduction of oxidative stress in people with ABCD. Research presented in this review was identified through searches of PubMed/Medline, EMBASE and the Cochrane Library databases. Observational studies report that people with ABCD have lower serum concentrations of antioxidants such as vitamins C, E and coenzyme Q10. Scientific evidence affirms that the use of antioxidants in the nutritional therapy of people with ABCD results in a decrease in prooxidative markers. In clinical practice, various factors such as diet, pharmacotherapy, stress levels and disease progression could reduce the efficacy of antioxidant compounds in the nutritional treatment of ABCD. The appropriate dosage of bioactive compounds with antioxidant effects results in a potential ally in the metabolic control of people with ABCD.
National Institute for Research and Education in Health and Nutrition, Yucatan, Mexico
Abigail Meza Peñafiel
National Institute for Research and Education in Health and Nutrition, Yucatan, Mexico
Danna Paola Mena Ortega
University Latino, Yucatan, Mexico
*Address all correspondence to: eemartinez.leo@gmail.com
1. Introduction
Adiposity-based chronic disease (ABCD) is an updated clinical diagnostic term for obesity, postulated in 2017 by the American Association of Clinical Endocrinologists (AACE) and the American College of Endocrinology. ABCD is a concept that focuses the disease on the deregulation of adipose tissue, to displace terms such as overweight and indicators such as body mass index (BMI) [1].
This new term and way of seeing and treating obesity acquire importance by eliminating weight as an indicator of diagnosis and control while viewing obesity as a disease whose development occurs due to the alteration of cellular oxidative processes, thus being the weight, only a clinical sign that underlies as a product of all the systemic alterations of oxidative stress and inflammation. This has led various research groups to develop new strategies for the clinical diagnosis and intervention of ABCD, based on its etiological components: oxidative stress and low-grade chronic inflammation [1].
In the last three decades, the number of people with ABCD has tripled, creating a global public health crisis. While in 2014 more than 2.5 billion adults aged 18 or over had ACBD, by 2020 the Global Nutrition Report reports that 1 in 3 people have ABCD [2].
The change in the eating pattern, usually characterized by an increase in the intake of simple carbohydrates and saturated fatty acids (SFA), as well as low consumption of antioxidants (Aox) from fresh vegetables is the beginning of cellular alterations at the level of adipose tissue and related organs that lead to the ABCD development [3].
Within the framework of the biochemical-metabolic alterations that give rise to ABCD development, mitochondrial dysfunction and oxidative stress point to the centre and connection point of metabolic diseases [4]. Derived from the above, the implementation of nutritional interventions based on the use of antioxidants seems to be an ally for the reduction of oxidative stress and metabolic control of people with ABCD.
ABCD is a complex and multifactorial disease of an inflammatory nature, characterized by excess storage of adipose tissue in the body and accompanied by metabolic alterations, which predispose to the presentation of other complex diseases, such as diabetes mellitus (DM), dyslipidemia, cardiovascular diseases (CVD), and some types of cancer, reducing the quality and life expectancy in 10 years [5, 6].
The excess energy that is stored in adipocytes favors an increase in size (hypertrophy) and/or in number (hyperplasia). This imbalance is the result of a combination of various physiological, psychological, metabolic, genetic, socioeconomic, cultural, and emotional factors. This translates into an increase in body weight, which is different for each person and social group [7].
One way to classify ECBA is according to the distribution of fat in the body:
Type 1: Fat/excessive weight distributed in all body regions.
Type 2: Excessive subcutaneous fat in the abdominal region, or android adiposity.
Type 3: Excessive deep abdominal fat.
Type 4: Excess fat in the gluteal and femoral regions, or gynecoid adiposity.
Usually, BMI is used which is a relationship between the weight and the height of the person; although this index is a very useful and easy-to-use parameter, it is mainly used for population studies, and it is not effective at the individual level, where there are other more important indicators [7].
Given the complexity of ABCD, the use of indicators and markers (Table 1) is currently suggested to allow knowing the status and evolution of this disease, based on the inflammatory process that characterizes it [8].
Variable
Standard parameter
Anthropometric indicators
body fat percentage abdominal circumference waist-hip ratio
W 20–25%; M 15–20% W ≤ 88 cm; M ≤ 102 cm W ≤ 0.75; M ≤ 0.85
Biochemical markers of inflammation
C-RP TNFα IL-6 uric acid
≤ 0.1 mg/dL 0–8.1 pg./mL 3.4–5.9 pg./mL W 3.4–7 mg/dL; M 2.4–6 mg/dL
In the present review, the scientific evidence on the clinical use of bioactive compounds with antioxidant effect in people with ABCD and the reduction of markers of oxidative stress is analyzed; from the search for information in the PubMed/Medline, EMBASE and Cochrane library databases, using as keywords: obesity, oxidative stress, antioxidants, mitochondrial dysfunction, and inflammation.
2. Chronic oxidative stress, a key point in the initiation of ACBD
The eating pattern has been studied by various research groups as an important risk factor in the development of metabolic diseases. Particularly, the high consumption of simple carbohydrates and the low consumption of antioxidant sources (vegetables and fruits) leads to important and key disturbances in ABCD development [9].
Initially, the high consumption of simple carbohydrates leads to an increase in blood glucose concentrations, which are regulated by various tissues, including skeletal muscle (SM). SM is a major, peripheral tissue of a metabolic nature, responsible for the regulation of blood glucose concentrations. Due to its rich content of mitochondria, it can efficiently metabolize glucose, producing intermediate metabolites (Acetyl-CoA) for other important pathways, adenosine triphosphate (ATP), carbon dioxide (CO2) and water (H2O) [10].
Physiologically, 98% of the oxygen (O2) that enters the mitochondria is used for the oxidative processes of Acetyl-CoA. The remaining 2% of O2 reacts spontaneously to form reactive oxygen species (ROS) that are subsequently broken down by antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (Gpx). This is an oxidative-reductive control mechanism that maintains the chemical homeostasis of the cell [11].
Chronic and increasing consumption of simple carbohydrates leads to the saturation of oxidative processes. This results in a decrease in physiological O2 and an increase in free O2 with the gradual reduction of oxidative metabolism and ATP production, collectively known as mitochondrial dysfunction. The ROS overproduction, derived from the increase in free O2, positively modulates the cellular antioxidant response; however, the decrease in the consumption of dietary antioxidants favors the oxidative-reductive imbalance. Thus, in an eating pattern that maintains a high consumption of simple carbohydrates and low consumption of antioxidants, it is the trigger for the exacerbated production of ROS and the decrease in antioxidant concentrations [12].
Oxidative stress is defined as the oxidative-reductive imbalance derived from high ROS concentrations and decreased cellular antioxidant concentrations. The oxidation-reduction disturbances produced in the mitochondria lead to the accumulation of pro-oxidative agents that damage macromolecular components, such as proteins and membrane lipids. Oxidation leads to irreversible damage and activation of death signals that compromise cell integrity and function [13].
The decrease in mitochondrial functions is the beginning of the cascade of disturbances that originates ACBD. As shown in Table 2, the oxidation of cell structures generates products whose elevation in the blood are biochemical markers of oxidation. Various studies reveal that high levels of oxidation products, such as malondialdehyde (MDA), oxidized very low-density lipoprotein (ox-LDL) and thiobarbituric acid reactive substances (TBARS), as well as low blood levels of vitamin C and E, are characteristic of people with ABCD [14, 15, 16].
Markers
Description
MDA
Oxidation products of AA, EPA and DHA fatty acids.
TBARS
Measurement of MDA formation.
8-epiPGF2
Derived from AA oxidation, the most representative is 8-epiPGF2.
oxLDL
Oxidative damage to the cholesterol transporter molecule.
Carbonyls
Result of the action of reactive species on amino acid side chains.
3-Nitrotyrosine
Result of the action of ROS on proteins.
Table 2.
Biochemical oxidation markers for oxidative stress.
The oxidative stress dissemination creates an environment conducive to inflammatory processes that disturb cellular homeostasis. The loss of cellular antioxidant function, together with lower consumption of antioxidants in the diet, produces the establishment of systemic oxidative stress. Due to the impact of oxidative stress on the development of biochemical alterations that give rise to ABCD, its evaluation, timely diagnosis and intervention are strategies for the metabolic control of ABCD.
Currently, the ABCD treatment base continues to prioritize weight loss; In addition to strategies without scientific evidence such as reductive massages among other relative techniques. This results in the development of complications and the so-called “rebound” which is the gain of lost weight and sometimes its doubling. These types of interventions minimize the importance of focusing on the origin of the disease. Although caloric restriction leads to weight reduction, it does not control the prooxidative state. Various studies on the effect of antioxidant dosage on ABCD show that high body fat is correlated with low antioxidant activities and high oxidative stress. For this reason, the use of bioactive compounds with antioxidant effects is an important ally for the control of oxidative stress [17, 18, 19, 20, 21, 22].
An antioxidant, by definition, can donate electrons to the unstable free radical to prevent the oxidation of other compounds. When an antioxidant donates its electrons, it becomes a free radical, but it cannot be reactive [23].
The role of dietary antioxidants in human health has been more extensively studied in recent years. Clinical and observational studies support the use of antioxidant therapy as an ally in the treatment of obesity. From the above, studies on the antioxidant effect of ascorbic acid, coenzyme Q10, and vitamin E have shown action on oxidative stress markers in people with obesity. Specifically, the importance of some antioxidants in clinical practice is described.
3.1 Ascorbic acid
L-ascorbic acid (AA), commonly called vitamin C, is considered one of the most potent antioxidant agents in the body. It is important in all stressful conditions that are linked to inflammatory processes and involve immunity. It is a water-soluble vitamin, with a six-carbon lactone chemical structure. It has two hydroxyl groups at the ends of a double bond between C2 and C3. It is a weak acid, relatively unstable in an alkaline medium and sensitive to heat (Figure 1). AA is found in all fruits and vegetables, especially citrus fruits, strawberries, cantaloupe, green peppers, tomatoes, broccoli, and leafy greens [24].
Figure 1.
Chemical structure of L-ascorbic acid.
AA exists mainly in two forms in vivo, ascorbic acid (reduced form) and dehydroascorbic acid (DHA) (oxidized form), of which the former is predominant. DHA has been shown to compete with glucose for transport via several glucose transporters, DHA uptake is expected to be inhibited by excess glucose, while the maximal rates of AA and DHA uptake are similar when no glucose [25].
AA is readily absorbed in the small intestine, specifically in the duodenum, using an active mechanism that requires two sodium-dependent transporters (SVCT1 and SVCT2). SVCT1 represents a high-capacity, low-affinity ascorbate transporter and is largely present in epithelial tissues, where it is involved in dietary ascorbate uptake and renal reabsorption, and SVCT2 is a low-capacity, high-affinity transporter widely expressed in all organs. Distribution from the bloodstream to different tissues is primarily governed by SVCT2. [24].
AA metabolism is closely linked to its antioxidant function through its enediol structure, serving as an efficient electron donor in biological reactions, supplying reducing equivalents as a cofactor or inhibitor of free radicals. The excretion will be mediated by the kidney in the form of DHA or oxalic acid, with the glomeruli being responsible for filtration into the lumen of the renal tubule [25].
Under normal conditions, adult humans have serum concentrations of 0.50–1.80 mg/dL or between 1500 and 3000 mg depending on the level of intake, and it is estimated that below 900 mg is considered a low concentration [26]. Among its multiple benefits, AA is effective in improving the immune system, in the absorption of non-heme iron and its transport, it is also a cofactor of approximately 15 different enzymes; plays a role in the production of collagen and the synthesis and metabolism of steroid hormones [27].
In people with ABCD, it is common to find AA deficiencies. Among its main functions compared to ABCD is that of a reducing agent and antioxidant; being a free radical scavenger and protecting tissues against oxidative stress [26]. According to Castillo et al. [28], there is a negative correlation between AA levels/body mass index, waist-height ratio, and leptin concentrations. A dose of 500–1000 mg/day for 1 month showed effectiveness in the levels of oxidative stress marker values in people with ABCD [29]. A dose of 1000 mg per day, for 4 months, decreased the oxidative stress marker 8-epiPGF2 and improved postprandial glucose. While high doses of 2000 mg for 8 weeks in people with ABCD produces a decrease in weight and BMI [30, 31].
3.2 Vitamin E
Vitamin E is an isoprenoid lipid from the tocopherol family. Its biologically active form is D–α tocopherol, whose phenolic hydroxyl on the chroman ring is responsible for antioxidant reduction (Figure 2). It is a lipophilic antioxidant that is in cell membranes, whose absorption and transport are closely linked to that of lipids [32].
Figure 2.
Chemical structure of D-α tocopherol.
The largest sources of α-tocopherol are found in wheat germ oil, almonds, sunflower oil, safflower oil, hazelnuts, and peanuts. Other important, but less well-known sources of α-tocopherol include pseudocereals such as quinoa, amaranth, lentils, and chickpeas [32].
Oral administration of vitamin E from natural sources results in the formation of micelles with bile acids, cholesterol, phospholipids, and triacylglycerol, allowing it to reach the intestinal lumen. These micelles are absorbed by intestinal cells. Within the enterocyte, vitamin E is esterified to chylomicron along with other dietary lipids. The resulting chylomicron form of vitamin E circulates through the lymphatic system into the bloodstream through the thoracic duct. The vitamin E-containing chylomicron reaches the liver before being absorbed by very low-density lipoprotein (VLDL) and released into the bloodstream. Likewise, hepatic catabolism mediated by cytochrome P450 (CYP) also contributes to the tissue distribution of tocotrienol. Vitamin E isomers are metabolized by side-chain degradation initiated by CYP-catalyzed hydroxylation followed by beta-oxidation [33].
Mainly, the action of vitamin E consists in protecting the polyunsaturated fatty acids of the phospholipids of the cell membrane from peroxidation and in inhibiting the peroxidation of LDL. Neutralizes singlet oxygen, captures hydroxyl free radicals, neutralizes peroxides, and captures superoxide anion to convert it to less reactive forms [33].
The use of vitamin E in the treatment of ABCD has been analyzed in various investigations, finding dosages ranging from 67 to 900 mg/day with a duration of 1 to 24 months. The consumption of 800 IU per day of vitamin E showed a decrease in oxidative stress markers and a decrease in proinflammatory cytokines in people with ACBD. Although there is still insufficient scientific evidence on the direct effect of vitamin E on reducing body weight in humans, a cross-sectional study demonstrated an inverse relationship between obesity and serum vitamin E level [34, 35].
3.3 Coenzyme Q10
Coenzyme Q10 (CoQ10) (2,3-dimethoxy-5-methyl-6-decaprenyl-benzoquinone) or ubiquinone in its oxidized form and ubiquinol in its reduced form, is synthesized from the mevalonate cycle obtained from the condensation of acetyl-CoA, responsible for the synthesis of cholesterol (Figure 3). Ubiquinol, the completely reduced form of CoQ10, is a lipophilic antioxidant capable of neutralizing free radicals and regenerating the reduced form of vitamin E. It is the only lipophilic antioxidant that can be synthesized by cells and that has enzymatic mechanisms to regenerate its reduced form [36].
Figure 3.
Chemical structure of coenzyme Q10 (ubiquinone).
CoQ10 is present in plants and animals, but its amount is higher in products of animal origin. Foods such as meat, poultry, and fish are the richest sources of CoQ10 in the diet [37]. After oral consumption, CoQ10 is absorbed by simple diffusion, through emulsification of bile salts. Upon entering the enterocyte, it is esterified to the chylomicron for transport and delivery to the liver. Subsequently, a distribution to the tissues is carried out through lipoproteins. Due to its important antioxidant function, tissues with high oxidative expenditure such as the heart, brain, kidney, and liver, are those with the highest concentrations of CoQ10. Its elimination phase is long, with a half-life of about 30 hours. The main route of elimination of CoQ10 is biliary and fecal excretion. The amount of time it takes for CoQ10 to reach a pharmacological steady state is quite long (1–2 weeks) [38, 39].
People with ABCD have decreased levels of CoQ10. The dosage of 100–300 mg/24 h of CoQ10 decreases the levels of hepatic gamma-glutamyl transferase and lactate dehydrogenase. In people with metabolic syndrome, the use of CoQ10 has effects on the levels of adiponectin, glucose, insulin and HOMA index [40]. Studied doses of 100 mg/day for 8 weeks, significantly reduce IL-6 and protein carbonyl (PCO) levels. According to Gholami et al. [41] a dose of 100 mg/day for 12 weeks reduces glucose, total cholesterol, and LDL levels, a fact reaffirmed by Farsi et al. [42] and Moasen et al. [43] that demonstrate positive effects on the reduction of oxidative stress markers.
3.4 Phenolic compounds
The term “phenols” encompasses approximately 8000 naturally occurring compounds. Many of these structures are found naturally in plants providing color and sensory characteristics. There are several classes and subclasses of polyphenols that are defined based on the number of phenolic rings that they possess and the structural elements that these rings present [44].
Flavonoids are phenols that constitute a very large group of compounds, of which more than 5000 are known. The main classes of flavonoids include others such, as flavones, flavonols, and isoflavones (Figure 4) [45]. The antioxidant activity of flavonoids results from a combination of their chelating properties of iron and scavengers of free radicals, thus avoiding the formation of reactive oxygen species. At the same time, they stimulate antioxidant enzymes catalase and superoxide dismutase [46].
Figure 4.
Chemical structure of phenolic compounds (a) flavone; (b) flavonol; (c) isoflavone.
Most polyphenols are present in food as esters, glycosides, or polymers, forms that cannot be absorbed. Once absorbed, polyphenols are subject to metabolic detoxification processes, which include different modifications such as methylation, sulfation, and glucuronidation. These processes increase the hydrophobicity of the compound and facilitate its excretion through the urine or bile. Polyphenols are distributed to those tissues where they have been metabolized and accumulate in specific target tissues, such as the lung, pancreatic, brain, and cardiac tissues [47].
The use of dietary polyphenols in the treatment of obesity has been studied. Specifically, habitual consumption of green tea in a population of 1210 adults showed a 2.1% reduction in waist-hip ratio and 19.6% in fat percentage, compared to the group that did not consume green tea [30]. According to Nagao et al. [48] the consumption of 580 mg of catechins presents a reduction in body weight, body fat index, hip circumference and BMI in subjects with ABCD. On the other hand, a randomized trial of 102 women with ABCD divided into 2 groups (green tea group with a dose of epigallocatechin-3-O-gallate (EGCG) of 857 mg per day and placebo group), showed after 12 weeks of consumption a significant weight loss, decrease in BMI, waist circumference, total cholesterol, and the level of low-density lipoproteins (LDL) without any side or adverse effects [49].
Based on multiple studies, the reduction in waist-to-hip ratio after green tea consumption is remarkably significant in subjects with a green tea dose of ≥800 mg/day with the average duration of treatment being 3 to 12 weeks. It is suggested that the average dose of green tea is 500 mg per day resulting in loss of body weight during 12 weeks of treatment [50]. Table 3 presents a summary of the main results obtained on the intervention of antioxidants in the ABCD treatment.
Antioxidant
Dose
Result
Reference
Ascorbic acid
1 g/day 4 months
Decreases marker of oxidative stress Isoprostane F2. Regulation of postprandial glucose levels. Insulin sensitivity
Weight loss by an average of 1.5 kg. Decreased percentage of fat by 2.5%. Decreased waist circumference by an average of 2.5 cm and hip circumference by an average of 2.3 cm.
4. Important considerations for the use of dietary antioxidants
Regardless of the contribution of antioxidants with nutraceuticals, the nutritionist must seek a natural source of bioactive compounds with potential antioxidant effects, through the consumption of fresh vegetables. The antioxidants present in food are “protected” through the food matrix; however, modifications to food (processing) can alter the antioxidant composition and therefore the biological effect. The use of dietary antioxidants must consider some important aspects to ensure the bioavailability and therapeutics of the antioxidant.
Specifically, hydrophilic antioxidants are thermolabile, therefore, in antioxidant therapy, the consumption of vegetables in the form of consommés, broths or any presentation that involves cooking the vegetable should be avoided and reduce its antioxidant content. Hydrophilic antioxidants are easily extracted by aqueous media, therefore, frozen vegetables, which generally go through freeze-drying processes (a preservation method that consists of dehydrating the vegetables), imply a loss of hydrophilic antioxidants, but not lipophilic ones.
On the other hand, lipophilic antioxidants are heat resistant, and even some, such as lycopene, require their activation by heat. A useful strategy in the use of these antioxidants is extraction in apolar media. The combination of lipophilic antioxidants with oils is a means of protecting oils from the effect of their use at high temperatures. The inclusion of fresh vegetables at different mealtimes, teas, such as cinnamon, or fruit infusions (without sugar) is a strategy for providing dietary antioxidants.
ABCD is a complex metabolic disease, whose etiology has an important pro-oxidative component. Scientific evidence confirms that people with ABCD have elevated serum concentrations of oxidative agents and decreased antioxidants. The clinical use of antioxidants in people with ABCD has positive effects on metabolic control. Antioxidants such as CoQ10, vitamin C, vitamin E and phenols have shown efficacy in markers such as fat percentage, BMI, waist circumference, adiponectin, HOMA index, among others. In clinical practice, the management of dietary antioxidants, together with supplementation, is an ally in the nutritional treatment of people with ABCD. Although more scientific evidence is still needed on the clinical use of antioxidants in people with ABCD, it is also necessary to develop instruments that allow the evaluation of oxidative stress for a better intervention plan.
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Written By
Edwin Enrique Martínez Leo, Abigail Meza Peñafiel and Danna Paola Mena Ortega
Submitted: 06 June 2023Reviewed: 24 July 2023Published: 25 September 2024
Open access peer-reviewed chapter
