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Technology And Children: A Negative Effect On Health?

Technology & ChildrenOne of the vagaries of parenthood is that we think we know more than our kids, enough to maintain a watchful eye over all they do and the places they go.  That might have been true before the advent of wireless technology and electronic media, but that’s an iffy proposition today.  Of course, the connected parent is concerned about his child’s safety and does all he can to ensure it.  But that idea transcends the physical, for the motivational, psychological and emotional dangers are ubiquitous.

Anything that has benefits, whether subjectively perceived or real, could be laden with risks.  Dr. Gwenn Schurgin O’Keeffe, detailing her research from a recent issue of Pediatrics and reporting to WebMD, feels that, “Some young people find the lure of social media difficult to resist, which can interfere with homework, sleep, and physical activity,” adding that, “Parents need to understand how their child is using social media so they can set appropriate limits.”   The element of internet risk is recognized by about half the parents interviewed, but only a fourth deems internet sites safe.  (WebMD. 3/28/11)

Concerning the children’s point of view, half admitted not to have spoken with their parents about their internet and social media activities.  Only four percent of parents realize that their kids log-on more than ten times a day, and twelve percent don’t even know their kids have a social account.  “Nurturing friendships and community engagement” are named as positive reasons to connect online, but the downsides of bullying and sexual inappropriateness receive equal attention.  Dr. O’Keeffe suggests that age thirteen is suitable for social interaction via the internet, agreeing with federal privacy rules outlined on some of the more popular networking sites, such as Facebook.  (O’Keeffe. 2011)

For years, health care professionals, teachers (especially PE teachers) and too few parents have been concerned with the amount of time their kids spend in front of the TV, which for many households had been an electronic babysitter from the get-go. While the Journal of Adolescence tells us that kids’ TV time hasn’t increased appreciably in the last fifty years (Marshall. 2006), their video game and social networking time has. Electronic sexual solicitation of underage youth is not as widespread as one would think from the reports (Ybarra. 2008), but that does not eliminate or reduce the risk.  Such solicitation is more likely to come through text messaging and in chat rooms, and harassment of one kind or another through instant messaging than through social networking sites (Ibid).

Nonetheless, kids spend more than seven hours a day, on average, in front of a screen.  Recent evidence raises concerns about media’s effects on aggression, sexual behavior, substance use, disordered eating, and academic difficulties.  Intense and regular parental involvement can increase the benefits and reduce the harm that media can have for a developing child and for adolescents.  (Strasburger. 2010)  Such anxieties are not limited to this side of the Atlantic or Pacific, either.  Online “addictions” were found to be related not only to aggression, but also to narcissistic personality traits and self-control, in studies conducted in Korea using international parameters.  (KIM. 2008)

The same kids who have problems with their peers at school or in the mall are likely to be the ones at risk for manipulation and targeting on the internet or smart phone.  Picking up signs of aberrant behavior are important, but we have to be vigilant.  Changes in behavior that include depression or aggression, delinquency or truancy, and becoming a loner or hanging with the wrong crowd are signals.  From the biomedical position, sedentary habits at a young age might just be able to predict health problems in adulthood.   Now, that’s another issue.  This topic should not entertain role reversal, even if your child is more adept at using the computer than you are.

References

http://www.webmd.com/parenting/news/20110328/social-networking-may-affect-kids-health
Social Networking May Affect Kids’ Health
Report Urges Parents to Communicate and Participate When Kids Socialize Online

Pediatrics Vol. 127 No. 4 April 1, 2011 pp. 800 -804
The Impact of Social Media on Children, Adolescents, and Families
Gwenn Schurgin O’Keeffe, MD, Kathleen Clarke-Pearson, MD,
Council on Communications and Media

J Adolesc. 2006 Jun;29(3):333-49. Epub 2005 Oct 21.
A descriptive epidemiology of screen-based media use in youth: a review and critique.
Marshall SJ, Gorely T, Biddle SJ.

Pediatrics Vol. 121 No. 2 February 1, 2008 pp. e350 -e357
How Risky Are Social Networking Sites? A Comparison of Places Online Where Youth Sexual Solicitation and Harassment Occurs
Michele L. Ybarra, MPH, PhD, Kimberly J. Mitchell, PhD

Pediatrics Vol. 125 No. 4 April 1, 2010 pp. 756 -767
Health Effects of Media on Children and Adolescents
Victor C. Strasburger, MDa, Amy B. Jordan, PhDb, Ed Donnerstein, PhDc

Eur Psychiatry. 2008 Apr;23(3):212-8. Epub 2007 Dec 31.
The relationship between online game addiction and aggression, self-control and narcissistic personality traits.
Kim EJ, Namkoong K, Ku T, Kim SJ.

Br J Sports Med. 2011 Sep;45(11):906-13.
Sedentary behaviour in youth.
Pate RR, Mitchell JA, Byun W, Dowda M.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Low Cholesterol And Mental Health

sad-eggsIf mental health is defined as a state of emotional and psychological well-being in which an individual is able to use his or her cognitive and emotional capabilities, function in society, and meet the ordinary demands of everyday life, then we need to take care of the garage in which this vehicle is kept.  Measures of depression and anxiety assess things such as self-disparagement, pessimism, lack of drive, apprehension, inability to relax, and irritability, to name a few.  Interestingly, these evaluations have demonstrated a relationship to low lipid and lipoprotein concentrations.

In work done at the end of the last century, an inverse association between mental challenges and total cholesterol and lipids was found.  That means when one goes up, the other goes down.  Testing young adult females, Duke University Medical Center discovered that women “…with low total cholesterol concentrations (<4.14 mmol/liter) relative to those with moderate to high cholesterol levels, were more likely to have higher scores on the NEO depression subscale…and anxiety subscale…” after adjustments were made for age, body mass index, oral contraceptive use and physical activity.  (Suarez.  1999)

Before we got too involved, it pays to know that 4.14 mmol/liter is equal to a cholesterol level of 160 mg/dL, or just plain 160.  Cholesterol is a steroid substance necessary to human life.  It forms the cell membranes in all organs and tissues of the body, is essential to the production of the hormones we need for growth, development, and reproduction, and it makes the bile acids necessary for absorption of nutrients.  Very little, if any, dietary cholesterol becomes serum cholesterol.

Back in the 1990’s it was noted that cholesterol levels below 160 were tied to excess mortality from all causes, primarily from a variety of cancers, respiratory and digestive diseases, and violent deaths from suicide and trauma.  Reasons behind low cholesterol have been ascribed to genetics, resistance to dietary sources, acute infections, and alcohol use/abuse.  (Meilahn.  1995)  If suicide is tied to depression, then it may be a legitimate effect.  Depression is twice as common among women as men, with about one in four suffering at some point in her lifetime.  The greatest vulnerability appears during the childbearing years, the time when its diagnosis is often overlooked.  The turbulence of hormones flooding a woman’s system at different times and in differing amounts can surely be a potent stressor.

Scientists in Barcelona, Spain, realized the connection of cholesterol to neuropsychiatric disease in a review of related literature that preceded their interest.  They found a link to early death, suicide and aggression, and personality disorders and dementia. (Martinez-Carpio.  2009). It appears that the good intentions of reducing what was thought to be the cause of cardiac mortality opened a different can of worms.  The Japanese explored the intrigue that was sparked when total mortality was not reduced despite reduction of mortality due to coronary heart disease, and found an increase in death rates due to suicide and accidents, many of which were tied to risky behaviors in persons with low cholesterol levels.  (Kunugi.  2001)  Does low cholesterol compromise judgment?  The U. of California conducted trials in the early 90’s to determine the cause behind the rise in suicides in men older than fifty years, and found that depression was three times more prevalent in those whose cholesterol was lower than 160.  Health status, number of chronic diseases, number of medications, and exercise seemed not to have had an adverse effect on depressive signs and symptoms. This led to the suggestion that the intentional lowering of cholesterol be more deliberate.  (Morgan. 1993)

Cedars-Sinai Medical Center, in Los Angeles, reported that serotonin, a neurotransmitter that controls impulsive behaviors, is tied to cholesterol levels at the synapses.  Low membrane cholesterol decreases the number of serotonin receptors, thereby reducing suppression of aggressive and destructive behaviors.  (Engelberg. 1992)  That magic number, 160, once again made headlines in the Netherlands, where epidemiologists discovered a higher prevalence of depression in males whose cholesterol was below that level.  (Steegmans. 2000)  Low cholesterol was cited as causative to rises in criminal violence in Sweden, following the association of reduced cholesterol values to low serotonin activity. (Golomb. 2000)  Reduced levels of total cholesterol, LDL, and HDL resulted in minimized serotonin values in personality disordered cocaine users, as reported by addiction researchers in their journal. (Buydens-Branchey. 2000)  In school-aged children, those with cholesterol values lower than 145 were three times more likely to have been suspended or expelled from school.  This is an absolute consideration, and has nothing to do with socio-economic status or ethnic background, nor with nutrition status or academic achievement.  (Zhang. 2005)

Life is supposed to be a balancing act.  Lots of us overdo something.  The balance between total cholesterol and HDL can allay fears of cardiovascular disease, despite cholesterol in the 200 range.  Cholesterol levels below 170 can make us irritable…and irritating.

References

Suarez EC.
Relations of trait depression and anxiety to low lipid and lipoprotein concentrations in healthy young adult women.
Psychosom Med. 1999 May-Jun;61(3):273-9.

Elaine N. Meilahn, MD
Low Serum Cholesterol  Hazardous to Health?
Circulation. 1995;92:2365-2366

Martínez-Carpio PA, Barba J, Bedoya-Del Campillo A.
[Relation between cholesterol levels and neuropsychiatric disorders].  [Article in Spanish]
Rev Neurol. 2009 Mar 1-15;48(5):261-4.

Kunugi H.
[Low serum cholesterol and suicidal behavior].  [Article in Japanese]
Nihon Rinsho. 2001 Aug;59(8):1599-604.

Morgan RE, Palinkas LA, Barrett-Connor EL, Wingard DL.
Plasma cholesterol and depressive symptoms in older men.
Lancet. 1993 Jan 9;341(8837):75-9.

Engelberg H.
Low serum cholesterol and suicide.
Lancet. 1992 Mar 21;339(8795):727-9.

Paul H. A. Steegmans, MD, Arno W. Hoes, MD, PhD, Annette A. A. Bak, MD, PhD, Emiel van der Does, MD, PhD and Diederick E. Grobbee, MD, PhD
Higher Prevalence of Depressive Symptoms in Middle-Aged Men With Low Serum Cholesterol Levels
Psychosomatic Medicine 62:205-211 (2000)

Beatrice A Golomb, Håkan Stattin, Sarnoff Mednick
Low cholesterol and violent crime
Journal of Psychiatric Research. Volume 34, Issue 4 , Pages 301-309, July 2000

Laure Buydens-Branchey, Marc Branchey, Jeffrey Hudson, Paul Fergeson
Low HDL cholesterol, aggression and altered central serotonergic activity
Psychiatry Research. Volume 93, Issue 2 , Pages 93-102, 6 March 2000

Zhang J, Muldoon MF, McKeown RE, Cuffe SP
Association of serum cholesterol and history of school suspension among school-age children and adolescents in the United States.
Am J Epidemiol 2005; 161:691-9.

Scanlon SM, Williams DC, Schloss P.
Membrane cholesterol modulates serotonin transporter activity
Biochemistry. 2001 Sep 4;40(35):10507-13.

Laure Buydens-Branchey,a Marc Branchey,a and Joseph R. Hibbelnb
ASSOCIATIONS BETWEEN INCREASES IN PLASMA N-3 POLYUNSATURATED FATTY ACIDS FOLLOWING SUPPLEMENTATION AND DECREASES IN ANGER AND ANXIETY IN SUBSTANCE ABUSERS
Prog Neuropsychopharmacol Biol Psychiatry. 2008 February 15; 32(2): 568–575.

BRIAN HALLAHAN, MRCPsych and MALCOLM R. GARLAND, MRCPsych
Essential fatty acids and mental health
The British Journal of Psychiatry (2005) 186: 275-277

Hillbrand M, Waite BM, Miller DS, Spitz RT, Lingswiler VM
Serum cholesterol concentrations and mood states in violent psychiatric patients: an experience sampling study.
J Behav Med 2000; 23:519-29.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Fructose Is an Inflammatory Word

corn-syrupInflammatory words arouse strong emotion. Related to our physical being, the term “inflammatory” refers to the body’s strong response to invasion by a foreign substance, such as a virus or bacterium, or to direct injury of tissue, both conditions stimulating the body’s attempt at self-protection with the ultimate goal of healing. Taking a closer look at the word “inflammation,” we see f-l-a-m, which suggests “flame.”  Now that you have the mental image, the defining characteristics of inflammation make sense—capillary dilation, leukocyte infiltration, redness, heat, and pain, all of which pull together to get rid of the damaging perpetrator.

Inflammation is not the same thing as infection, even when infection causes inflammation. Ongoing inflammation can self-perpetuate, particularly if there is a gene variant linked to it. If swelling is visible, our first reaction is to stop it, but not all inflammation is so apparent. This invisible inflammation, at the low end of the spectrum, is usually present for a long time and is termed “chronic.”  We know of its presence because it can be seen under a microscope or through specialized blood tests, such as highly-sensitive C-reactive protein or erythrocyte sedimentation rate (ESR). This inflammation, some believe, is the basis of degenerative diseases, including cardiovascular disease, diabetes, certain forms of cancer, Parkinson’s and Alzheimer’s, autoimmune diseases, and even wrinkled, sagging skin. Although inflammation is necessary for healing, it needs to stop once the healing is accomplished.

While there are drugs and over-the-counter medicines that can tame inflammation, they come with serious side effects when used long term. An easier solution is to reduce chronic inflammation through diet. Sugars are pro-inflammatory. Refined grains that cause glucose and insulin spikes are pro-inflammatory. Rancid, processed vegetable oils are pro-inflammatory. Processed foods and their trans-fats are pro-inflammatory. Among the most reliably pro-inflammatory molecules, though, is fructose. Common to soft drinks and fruit juices—and to the fruits from which they are extracted—sucrose puts people at risk for depleting their stores of critically important ATP (Abdelmalek, 2012), which provides energy for cellular processes. Unlike other simple sugars, fructose requires ATP for its metabolism, the depletion of which increases risk for inflammation, especially in the liver, where non-alcoholic fatty liver disease may follow (Ouyang, 2008). Additionally, Abdelmalek and colleagues determined that more uric acid is produced when excess fructose is consumed, increasing the odds for suffering gout, elevated blood pressure, type 2 diabetes, metabolic syndrome, and uric-acid- related kidney stones (Abdelmalek, 2012). The moderate intake of fructose from fresh fruits is not so much a concern because of their concomitant fiber and micronutrients.

Endothelial cells make up the thin layer of cells that line the interior of blood and lymphatic vessels. Vascular endothelial cells line the entire circulatory system, from the heart to the tiniest capillaries. Dysfunction of these cells sets the stage for vascular diseases, and is considered a key to the development of atherosclerosis. Such can be initiated by inflammation, which can be induced by fructose (Glushakova, 2008). The response to fructose might also include a cascade of events that leads to the progression of kidney disease and the incidence of metabolic syndrome (Choi, 2009). Where kidneys are concerned, control of blood pressure is important, since the angiotensin-renin system depends upon the kidneys for regulation and adjustment of arterial pressure. A diet low in fructose improves blood pressure and inflammatory markers, especially for those whose lifestyles or genetics increase risk for kidney disease (Brymora, 2012).

Fructose is absorbed directly by the intestine. If combined with glucose, as it is in table sugar (sucrose), enzymes will separate it and it will be absorbed like free fructose. It gets taken up by the liver and does not require insulin for metabolism, so it is not burned inside cells. It does get stored as fat, though, and does increase triglycerides (Kaumi, 1996). But it’s hard to imagine fructose being related to kidney stones.  Sparked by an interest in the burgeoning consumption of fructose in recent decades, researchers at Harvard found that fructose increases the urinary excretion of oxalates, uric acid and other factors associated with kidney stone formation. Though the fructose bound to glucose in table sugar was not exculpated, the freed fructose is independently associated with increased risk for stones (Taylor, 2008) (Cirillo, 2009).

For those so inclined, addictions share cross-overs much as training regimens do for athletes.  Alcohol dependence has not only genetic factors, but also psychosocial and environmental factors that can lead to prolonged periods of heavy alcohol consumption.  Sooner or later, withdrawal symptoms telegraph physical dependence, which instigates a variety of social and/or legal problems. Children adopted away from an alcoholic history still have the risk. Fructose is fermentable to ethanol. Close observation of fructose metabolism in the liver and activity in the brain shows parallelism with ethanol. First, both serve as substrates for lipid manufacture and the promotion of hepatic insulin resistance, dyslipidemia and steatosis. Second, fructose will cross-link with proteins to form acetaldehyde, which is an intermediate in the metabolism of alcohol that causes headaches and irritation to mucous membranes, among other disasters. But the third common element might be the worst. The hedonic center of the brain is stimulated by fructose in the same manner as alcohol, creating habituation and maybe even dependence (Lustig, 2010) (Byerley, 2010). Obesity is not an innocuous sequela to fructose overdose. But a least there are no traffic tickets for driving fat.

Triglycerides go up. Advanced glycation end products make cell membranes brittle and dysfunctional. Inflamed kidneys respond by forming stones. Blood pressure may rise. The liver collects fatty deposits made from triglycerides. Insulin resistance can lead to type 2 diabetes. Inflammation by fructose.

Some of the people you see are walking masses of inflammation, a maelstrom of metabolic mélange modulated by mouth. We might not have the right to intervene, but we can set an example.

References

Abdelmalek MF, Lazo M, Horska A, Bonekamp S, Lipkin EW, Balasubramanyam A, Bantle JP, et al
Higher dietary fructose is associated with impaired hepatic adenosine triphosphate homeostasis in obese individuals with type 2 diabetes.
Hepatology. 2012 Sep;56(3):952-60.

Benetti E, Mastrocola R, Rogazzo M, Chiazza F, Aragno M, Fantozzi R, Collino M, Minetto MA.
High Sugar Intake and Development of Skeletal Muscle Insulin Resistance and Inflammation in Mice: A Protective Role for PPAR- δ Agonism.
Mediators Inflamm. 2013;2013:509502.

Andrzej Brymora, Mariusz Flisiński, Richard J. Johnson, Grażzyna Goszka, Anna Stefańska, Jacek Manitius
Low-fructose Diet Lowers Blood Pressure and Inflammation in Patients With Chronic Kidney Disease
Nephrol Dial Transplant. 2012;27(2):608-612.

Byerley LO, Lee WN.
Are ethanol and fructose similar?
J Am Diet Assoc. 2010 Sep;110(9):1300-1.

Hyon K Choi, Gary Curhan
Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study
BMJ 2008;336:309

Mary E. Choi
The Not-so-Sweet Side of Fructose
JASN. March 2009; vol. 20 no. 3: 457-459

Cirillo P, Gersch MS, Mu W, Scherer PM, Kim KM, Gesualdo L, Henderson GN, Johnson RJ, Sautin YY.
Ketohexokinase-dependent metabolism of fructose induces proinflammatory mediators in proximal tubular cells.
J Am Soc Nephrol. 2009 Mar;20(3):545-53.

Collino M, Benetti E, Rogazzo M, Mastrocola R, Yaqoob MM, Aragno M, Thiemermann C, Fantozzi R.
Reversal of the deleterious effects of chronic dietary HFCS-55 intake by PPAR-δ agonism correlates with impaired NLRP3 inflammasome activation.
Biochem Pharmacol. 2013 Jan 15;85(2):257-64.

Glushakova O, Kosugi T, Roncal C, Mu W, Heinig M, Cirillo P, Sánchez-Lozada LG, et al
Fructose induces the inflammatory molecule ICAM-1 in endothelial cells.
J Am Soc Nephrol. 2008 Sep;19(9):1712-20.

Helen Hermana M Hermsdorff, María Ángeles Zulet, Blanca Puchau and José Alfredo Martínez
Fruit and vegetable consumption and proinflammatory gene expression from peripheral blood mononuclear cells in young adults: a translational study
Nutrition & Metabolism 2010, 7:42

Chidambaram Jaya, Vetriselvi Venkatesan­, Carani Venkatraman Anuradha
Inflammatory responses in liver induced by high fat plus fructose diet: therapeutic potential of cissus quadrangularis stem
Int J Biol Med Res. 2010; 1(4): 120 – 124

Johnson RJ, Sanchez-Lozada LG, Nakagawa T.
The effect of fructose on renal biology and disease.
J Am Soc Nephrol. 2010 Dec;21(12):2036-9.

Kaumi T, Hirano T, Odaka H, Ebara T, Amano N, Hozumi T, Ishida Y, Yoshino G.
VLDL triglyceride kinetics in Wistar fatty rats, an animal model of NIDDM: effects of dietary fructose alone or in combination with pioglitazone.
Diabetes. 1996 Jun;45(6):806-11.

Lê KA, Tappy L.
Metabolic effects of fructose.
Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):469-75.

Lustig RH.
Fructose: metabolic, hedonic, and societal parallels with ethanol.
J Am Diet Assoc. 2010 Sep;110(9):1307-21.

Mattioli LF, Thomas JH, Holloway NB, Schropp KP, Wood JG.
Effects of intragastric fructose and dextrose on mesenteric microvascular inflammation and postprandial hyperemia in the rat.
JPEN J Parenter Enteral Nutr. 2011 Mar;35(2):223-8.

Ouyang X, Cirillo P, Sautin Y, McCall S, Bruchette JL, Diehl AM, Johnson RJ, Abdelmalek MF.
Fructose consumption as a risk factor for non-alcoholic fatty liver disease.
J Hepatol. 2008 Jun;48(6):993-9.

Rayssiguier Y, Gueux E, Nowacki W, Rock E, Mazur
High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation.
Magnes Res. 2006 Dec;19(4):237-43.

Seaman DR.
The diet-induced proinflammatory state: a cause of chronic pain and other degenerative diseases?
J Manipulative Physiol Ther. 2002 Mar-Apr;25(3):168-79.

Taylor EN, Curhan GC.
Fructose consumption and the risk of kidney stones.
Kidney Int. 2008 Jan;73(2):207-12.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.