
However, “the combination and/or interaction of dietary protein, calcium from dairy and the additional vitamin D that fortifies dairy products appears to protect bone health during weight loss,” said lead study author Matthew Thorpe. Social media is awash with all sorts of ways you can incorporate cottage cheese into your diet — and for good reason. Nonfat and low-fat cottage cheese are high in protein, which aids in weight loss around the midsection. It’s also packed with calcium, which can help prevent bone loss, which often goes hand in hand with weight loss. Accumulating research finds that extra weight in the midsection is linked to a number of health issues, from heart disease and type 2 diabetes to cancer and more.

Results of neurobehavioral investigations tend to support the view that aging increases one’s vulnerability to alcoholism-related decline (Oscar-Berman and Marinkovic 2003). Significant correlations have been reported between age and regional MRI and DTI measures and performance on working memory, visuospatial ability, and gait and balance (Pfefferbaum et al. 2006), as well as in interhemispheric processing speed (Schulte et al. 2005). The latter findings provide evidence alcoohol is better than drugs for the functional ramifications of an interaction of age and alcoholism in exerting compounded abnormalities in the functioning of the corpus callosum. One effect of chronic alcoholism is the damage that long-term heavy alcohol consumption does to the brain. Certain regions in the brains of alcoholics shrink, creating lesions that result in deficits in brain function. The figure is a composite of images from several functional magnetic resonance imaging (fMRI) studies.
These results suggests that certain functional differences in reward processing may predate problematic alcohol consumption. Risky drinking patterns for men are defined as consuming more than 14 drinks per week, or more than four drinks in a single day at least once a month; for women, the limits are more than seven drinks per week and three drinks per day (Dawson et al. 2005). Individuals who abuse alcohol or are alcohol-dependent are considered to have alcohol use disorder (Grant et al. 2004). Alcohol abuse, as described by the American Psychiatric Association (APA 1994), is a psychiatric condition whereby alcoholic beverages are consumed despite negative consequences for health, well being, and interpersonal relationships. Alcohol dependence has additional physiological consequences such as increased tolerance for alcohol consumed, and withdrawal symptoms upon cessation of drinking.
Specifically, Gsk3β in the mPFC participates in mechanisms underlying motivation to consume alcohol and alcohol withdrawal-induced anxiety [58]. Furthermore, genetic analysis in humans indicated that GSK3β is an alcohol dependence risk factor, suggesting a central role of GSK3β in AUD [58]. Surprisingly however, Gsk3β in the NAc is inhibited by alcohol in rats [40], emphasizing the region-specificity of alcohol’s action. Alcohol-dependent activation of mTORC2 in the DMS promotes F-actin assembly, the formation for mature spines and alcohol intake [59]. Neuropathological studies performed on the brains of deceased patients have revealed decreased neuron density in the frontal cortex of alcoholics (Harper and Matsumoto 2005).

As a part of a wider array of interrelated abnormalities, it has been shown that the hypothalamic–pituitary–adrenocortical (HPA) function is hyporeactive in chronic alcoholics (Errico et al. 2002; Lovallo 2006). Cortisol, in turn, increases mesencephalic dopaminergic transmission that underlies the activation of alcohol-induced brain reward circuitry (Bowirrat and Oscar-Berman 2005; Gianoulakis 1998; Piazza et al. 1996), in which the amygdala plays an essential role (Koob 2003). These additional abnormalities reflect widespread cerebral atrophy accompanying sustained alcohol abuse. Thus, consideration should be given to sensory and cognitive deficits that may be integral to the disease process caused by chronic alcoholism. It is a common belief that alcohol ingestion leads to aggression and reduced impulse control, and there is high association of alcohol intoxication with violent crimes (Murdoch et al. 1990). Results of laboratory research have shown that alcohol intoxication increases the likelihood of aggressive behaviors (Bushman and Cooper 1990; Hoaken and Stewart 2003).
However, the extent of alcohol induced microglial activation may well be dependent on the extent and pattern of alcohol exposure. Neuroimaging studies that measured gender differences in alcoholics’ brain functioning have yielded contradictory evidence, with some studies showing women to be more susceptible than men to brain impairments, and other studies showing no such distinction. Using functional magnetic resonance imaging (fMRI), Tapert et al. (2001) found decreased activity in parietal and frontal cortex, particularly in the right hemisphere, in alcohol-dependent women during performance of a spatial working memory task. Other studies, however, did not find functional https://ecosoberhouse.com/article/alcohol-and-headaches-why-does-alcohol-cause-migraines/ differences based on gender (Wang et al. 1998), or even found that alcohol intoxication decreased brain metabolism in men more than in women as measured with positron emission tomography (PET; Wang et al. 2003). Using structural MRI, Kroft et al. (1991) found that the average ventricular volume in alcoholic women was within the typical range found in MRI studies of nonalcoholic women of similar ages. Another MRI study reported that although age and alcoholism interacted adversely in both sexes, alcoholic men, but not alcoholic women, had abnormal cortical white matter and sulcal volumes compared to same sex healthy comparison groups (Pfefferbaum et al. 2001b).
