L’overdose di cibo “supergrasso” trasforma i globuli rossi

Fonte: La Repubblica (articolo originale)

Avete presente un globulo rosso, la cellula dal sangue che grazie all’emoglobina contenuta trasporta l’ossigeno a tutto l’organismo?
Nel corpo umano ce ne sono miliardi di miliardi e, tra le loro funzioni, c’è anche la regolazione della disponibilità di ossido nitrico che aiuta le arterie a mantenersi elastiche e quindi a dilatarsi in caso di bisogno.
Ma quanta differenza esiste tra un globulo rosso di una stessa persona prima e dopo un pasto ricchissimo in grassi.
Basta un solo appuntamento con questo tipo di cibo per rendere queste cellule più piccole e modificarne la forma.
Infatti, un carico in acuto di cibo grasso creerebbe veri e propri “spuntoni” sulla superficie dei globuli rossi, capaci non solo di modificarne la forma ma anche di “alterare” la loro funzione.

Tutte queste trasformazioni negative, presumibilmente temporanee, si osservano dopo una sola overdose di grassi alimentari.
A dimostrarlo è una ricerca apparsa su Laboratory Investigation e condotta dagli scienziati del Medical College della Georgia, di Augusta.
Lo studio, coordinato da Tyler W. Benson, è estremamente semplice.
Sono stati presi in esame dieci uomini che facevano regolare attività fisica e che avevano valori di colesterolo e trigliceridi del sangue perfettamente nella norma.
Poi sono stati fatti due gruppi da cinque.
Nel primo, i volontari hanno assunto una sorta di “beverone” ad altissimo contenuto in grassi, con un calcolo delle calorie proporzionato al fisico del soggetto, una sorta di pasto “iperlipidico” spinto.
Nel secondo invece, pur se con lo stesso quantitativo calorico, l’apporto nutrizionale in lipidi era estremamente ridotto e compensato da carboidrati e proteine.
Dopo quattro ore dal pasto sono stati fatti gli esami del sangue, gli scienziati si sono concentrati in particolare sulle caratteristiche dei globuli rossi e sono apparse le sorprese sotto forma di una riduzione della dimensione e un cambio della loro forma.
Sono comparsi infatti dei globuli rossi caratterizzati da un bordo “frastagliato”, presumibilmente meno capaci di viaggiare nei vasi sanguinei più piccoli, dove queste cellule consegnano normalmente il loro carico di ossigeno.

Inoltre, è bastata un’unica overdose alimentare di lipidi per notare un altro fenomeno potenzialmente negativo per il cuore: l’eccesso concentrato di grasso alimentare ha indotto un aumento della mieloperossidasi, enzima che già in passato ha dimostrato di influenzare l’elasticità delle arterie e l’ossidazione del colesterolo HDL, a tutto vantaggio di quello “cattivo” o LDL.

«Questo studio è interessante - segnala Pablo Werba, responsabile dell’Unità Prevenzione Aterosclerosi del Centro Cardiologico Monzino, IRCCS di Milano - perché scopre possibili meccanismi alla base dell’insorgenza “inaspettata” di problemi coronarici, come l’angina o l’infarto del miocardio, dopo un’abbuffata di cibo grasso.
Le evidenze emerse ci suggeriscono di considerare anche questo eccesso insieme agli altri comportamenti più noti che possono scatenare eventi cardiaci, come gli episodi di ira o gli sforzi fisici esagerati e inconsueti».

Insomma: l’eccesso di grasso alimentare può risultare davvero uno stress per il sangue e per il cuore. Quindi, meglio evitare overdose di cibo ipergrasso.

High Blood Sugar Linked to Prostate Enlargement, Low Testosterone and Prostate Cancer

(Source: http://www.drmirkin.com/men/high-blood-sugar-linked-to-prostate-enlargement-low-testosterone-and-prostate-cancer.html)

Metabolic syndrome and type II diabetes are characterized by high blood sugar, insulin, and triglycerides, low HDL and a fatty liver and obesity. Of 490 male adults, average age 58 years old, 37 percent with lower urinary tract obstruction (LUTS) had metabolic syndrome (Adv Urol, published online Jan 23, 2014). Of those with:
• mild LUTS, 37.4 percent had metabolic syndrome,
• moderate LUTS , 46.5 percent had metabolic syndrome and
• severe LUTS, 54.1 percent had metabolic syndrome.
The patients with metabolic syndrome had much larger prostates than those who did not have that syndrome. Obese men and those with higher levels of the bad LDL cholesterol also had larger prostates.

Low Testosterone and Prostate Cancer Linked to Metabolic Syndrome

Of 1,150 men aged 30 years or older, the lower the testosterone, the more likely a man is to have metabolic syndrome. (Urology, published online October 08, 2013). The researchers defined Metabolic Syndrome as a waist circumference of 85 cm or more plus any two of the following: triglyceride 150 mg/dl or higher, good HDL cholesterol level below 40 mg/dL, taking statins, systolic blood pressure of 130 mm Hg or higher, diastolic blood pressure of 85 mm Hg or higher, taking high blood pressure medications, fasting blood sugar 110 mg/dL or higher, or use of a drug to lower high blood sugar.

Men who had any three of the risk factors for metabolic syndrome are one and a half times more likely to develop prostate cancer than those who do not have metabolic syndrome (European Urology, published online February 24, 2014).

Metabolic Syndrome and Diabetes

Metabolic syndrome means you are on your way to becoming diabetic. Diabetes is a disease in which high blood sugar levels damage every cell in your body. When blood sugar levels rise too high (high blood sugar), the pancreas releases large amounts of insulin (high insulin), which converts sugar to a type of fat called triglycerides (high triglycerides). Then your body uses up its good HDL cholesterol to carry triglycerides from the bloodstream to the liver (low HDL). Next, the extra triglycerides carried to the liver are stored in the liver to form a fatty liver. The triglycerides are also stored in your body to make you fat (overweight). These are the components of both metabolic syndrome and Type II diabetes.

How 'Good Cholesterol' Stops Inflammation

From ScienceDaily website (see original article)

Dec. 9, 2013 — High cholesterol levels are seen as a cause of dangerous deposits in the bloodstream, which lead to hardening of the arteries (atherosclerosis).
As a consequence, thrombosis, strokes, and heart attacks can develop, which are among the leading causes of death in Western society.
Low-density lipoprotein (LDL) is commonly referred to as the "bad cholesterol," because it promotes atherosclerosis.
In contrast, the "good cholesterol," high-density lipoprotein (HDL), helps transport excess cholesterol out of the bloodstream and can counteract an inflammatory reaction in damaged vessel walls.

"It has long been known that HDL has a protective function in cardiovascular diseases that are based on atherosclerosis," reports Prof. Eicke Latz, Director of the Institute of Innate Immunity at the University of Bonn and who is further affiliated with the German Center for Neurodegenerative Diseases (DZNE) and the University of Massachusetts Medical School in the USA.
"The molecular causes to which this protective effect of HDL can be attributed were unclear until now."
For instance, studies had shown that therapies that simply increase HDL levels in the blood of patients are not sufficient to reduce the incidence of atherosclerosis.
HDL has anti-inflammatory effects on immune cells -- however the mechanisms have remained unclear until now.
The research group has now investigated how HDL acts upon inflammatory processes.

Bioinformatics approach revealed a candidate gene

Principle investigators Dr. Dominic De Nardo and Larisa I. Labzin are both Australians currently training in the lab of Prof. Eicke Latz.
In collaboration with other working groups of the University of Bonn, an international research team from Japan, Australia, China, the USA, and Germany has identified how HDL acts to prevent chronic inflammation.
In a very extensive study over a period of about three years, the group performed experiments in human and mouse cells, to determine which genes are regulated by high HDL levels.
"At first, we were really just feeling around in the dark," reports Prof. Latz.
Close cooperation with the working group of Prof. Joachim L. Schultze of the Life and Medical Sciences (LIMES) Institute of the University of Bonn finally got the scientists on the right track.
"With the aid of genomic and bioinformatics approaches, we were able to filter out a candidate gene from the wealth of regulated genes," adds Prof. Schultze.

This gene is found in phagocytes, which act in the body like police on the beat and, as part of the innate immune defense system, arrest intruders.
These patrolmen are supported by a kind of "criminal file," the so-called Toll-like receptors (TLR).
With their help, the phagocytes can distinguish between "good" and "bad."
If it is a dangerous intruder, the TLR can also trigger the release of inflammatory substances via biochemical signaling pathways.
The transcriptional regulator, ATF3, plays a key role in this process.
"It reduces the transcription of the inflammatory genes and prevents further stimulation of inflammatory processes via the Toll-like receptors," explains Dr. Dominic De Nardo.

Sustained inflammatory reactions can lead to organ failure

The immune system uses inflammatory processes to keep pathogens in check, to detect damaged tissue, and then repair it.
In sustained inflammatory reactions, however, there are dangerous consequences -including blood poisoning or organ failure.
"The transcriptional regulator ATF3 acts to reduce these inflammatory reactions by suppressing the activation of inflammatory genes following excessive stimulation of immunoreceptors," reports Dr. De Nardo.
In the end, high-density lipoprotein (HDL) is responsible for down regulating the inflammatory reactions, via the activation of ATF3.
"To put it simply, high HDL levels in blood are an important protective factor against sustained inflammation," summarizes Prof. Latz.

"Our studies also indicate that the amount of HDL in blood alone is not decisive for the protective function of HDL, but that the anti-inflammatory function is probably more important.
These results also suggest a molecular approach for treating inflammation in other widespread diseases, such as diabetes," sums up Prof. Latz.