First two commenters here are shadowbanned.
'Worryingly there is evidence that parents may be underestimating their daughters' mental health needs,' she added. 'Conversely, parents may be picking up on symptoms in their sons, which boys don't report themselves. It's vital that both children and their parents can make their voices heard to maximise the chances of early identification and access to specialist support.'
While the survey study makes some interesting findings, these types of conclusions make me quite skeptical especially in light of the fact that these are not clinical diagnosis for depression, but rather self-reported survey responses.
The claim that parents are better able to identify depressive symptoms in boys and underestimate them in girls does not seem to causally follow the results of a survey, even though it is multi-year (over a decade) for two main reasons.
One, a clinical diagnosis involves blood work to test for a bevy of diseases that are known to contribute to depression, in addition to the interviews. Also, the symptoms of depression are often confounded by the symptoms of other diseases, poor lifestyle choices, etc.
Secondly, the article neglects to mention one key aspect that is different in girls than boys, and it is the fact that girls undergo puberty earlier than boys, and so far the study has only published the 2012 Age 11 findings. Yet the scientist in the article is making a blanket statement speculating the difference between depression rates in girls (25%) and boys (10%) up to the age of 11 is primarily due to how parents treat either sex while completely neglecting the onset of puberty?
It is still a great study in terms of sample size and data collection, but let's let the Age 14 data be reviewed and published before jumping to conclusions just yet.
Science AMA Series: I'm Mark Dallas, a Lecturer in Cellular and Molecular Neuroscience at the School of Pharmacy, University of Reading. I carry out research to better understand what goes wrong in our brains in complex diseases such as Alzheimer’s disease and I’m here today to talk about it. AMA!
My name is Mark Dallas, I am a Lecturer in Cellular and Molecular Neuroscience at the School of Pharmacy, University of Reading, where I have worked for 4 years, after postdoctoral positions at the University of Leeds. I am Academic Co-ordinator for the Alzheimer’s Research UK Oxford Network, Neuroscience Theme Lead for the Physiological Society and on the editorial board of Physiology News.
My main research interest is working to understand the mechanism by which our brains change that leads to devastating diseases such as Alzheimer’s disease. Today 850,000 people in the UK live with dementia, and currently there is not treatment that will prevent, cure or slow down it’s progression. My experiments are looking at the so called glial cells within the brain and how they respond in the face of stressful stimuli. I believe these non-neuronal cells could provide insight and even early indications as to the onset of disease, well before clinical symptoms. Here we use a diverse array of model systems for cultured cells to animal models of disease. Only by building from cells to systems will we truly understand what is happening in our brains, the most complex computer of all.
It is my opinion that we still need some animal research to undercover the complexities of the brain and this research should be in concert with other non-animal experimental approaches. This will be fundamental to our research efforts aimed at combating Alzheimer’s disease. I wholly support the research community’s efforts to carry out this research under strict guidance that ensures responsible, high-quality research and requires the highest possible welfare standards, driven by application of the 3Rs. Indeed as part of my own research we are exploring the use of human cells as more appropriate models of brain disease.
Only by engaging the public in our research activities and how we use animals in science, will we address concerns and misunderstandings. This is something I am actively involved in through many outreach activities, including today.
During World Alzheimer’s Month, I’m here to talk about the wonders of our brains, and how they are disrupted by disease, what research is telling us about Alzheimer’s disease, the use of animal research in tackling human diseases, and I'll be back to answer questions at 10 AM ET (3 pm BST), Ask Me Anything!
This AMA is organised by Understanding Animal Research.
You mention that it is important to talk about how we use animals in science. What do you mean by that? What are the common misconceptions about animal model work?
Thank you for doing this AMA!
My understanding is that exercise is protective for aging brains, both in the presence and the absence of diseases such as Alzheimer's. Is that still a pretty well-supported view? Since many rodent animal models seem to live their lives in the absence of exercise opportunities, is this something we should push to change in how lab research is conducted . . . or maybe that makes them a better model for a lot of us?
Hi Mark, and thank you for doing this AMA!
What are your thoughts on "Type 3 diabetes" in the context of Alzheimer's disease?
How robust is the research that suggests that insulin resistance in the brain is occurring in a sizable fraction of AD patients?
What are the implications for synaptic health (synapses use lots of glucose)?
Is there a biological mechanism by which you can envision brain insulin resistance being linked to cognitive impairment?
Thanks for doing this AMA!
With both sides of my family with a history of Alzheimer's, I ask this with some self-interest. I've been following the resent research on the development of novel treatments, vaccines and genetic therapies.
I'll ask the obvious question - how close are we to a cure?
Thanks in advance!
Doesn't lack of sleep increase anxiety though?
Totally. This whole article is funny and never goes into the details of the actual findings.
If you have a normal sleep schedule over a long period of time, and feel depressed, one night of 3 hour sleep will likely help.
Regular sleep deprivation, however, does not aid you. In fact, it absolutely contributes to depression and anxiety.
I know it's only through personal observation, but this is why my depression gave me insomnia. I would feel so much better and more ... myself when I was sleep deprived. I would consistently do all nighters because I would always feel better on the second day. I hated waking up in the morning because I would feel the absolute worst then.
Keep in mind, this is a meta-analysis - not an original study. Data from previous sleep studies was compiled and researchers saw that half of the sleep deprived individuals had reduced depression. But they don't know why, under what conditions, what particular factors are different between people with reduced depression vs those with no change vs those with increased depression.
Take this with a grain of salt is all I'm saying. There are a lot of unknowns.
I don't want to read this. Anyone want to tl;dr it for me?
I want to read this. Anybody have access to the abstract?
From what I can tell of the summary, it's basically just the title. Fasting every other day promoted the development of beige fat in mice. Beige fat being a mix of white (storing energy) and brown (burning up energy for heat) fat, which I guess is healthier for you than just white fat.
Is it just fasting every other day, or the 18 hour fast and 6 hour feeding window that I generally associate with IF?
Does anyone else worry about the security implications of introducing quantum processing power to our current computing infrastructure? It seems like brute forcing would be taken to a whole other level.
Fortunately post-quantum cryptography is already pretty well developed, but unfortunately, it has not been tested by direct quantum computing brute force attacks as of yet.
Larger passwords = more quantum proof
A brute-force attack by a quantum computer will necessarily use the Grover Search algorithm, which has been proven to be the most efficient quantum search algorithm. Grover Search is based on an amplitude-amplification system which raises the probability-amplitude of the system collapsing into the 'right' answer by 1/(sqrt(N)), where N is the number of terms the algorithm searches through. Repeat this process sqrt(N) times, and the probability will be ~100%. Therefore, quantum-proof cryptography will probably be based on the difficulty of brute-force searches with twice as many bits as we use today. We don't really need to test this to know it will work.
How did they measure social conservatism? I can't very easily get past the paywall on my phone, but did anyone actually read the Methods section?
Edit: Apparently, they used a 12-item conservatism scale by Everett.
Here's a great example of where the actual paper should be read instead of just looking at the headline.
From the methods section of the paper:
Considering potential data loss, 523 Amazon Mechanical Turk workers participated in exchange for money. Participants who did not complete the survey and those with an IP outside of the U.S.A. were excluded, resulting in 426 participants.
I'm always wary of research studies that utilize web-surveys for their data collection. And especially wary of studies that utilize MTurk, which is predominately children pretending to be adults or someone based outside the US using a proxy and clicking through a 25-30 minute survey as fast as they can to earn anywhere from $0.50-$3. What they have here is not a representative sample of Americans, they have a representative sample of MTurk users using the site through a US IP address.
Perhaps it is this flawed methodology that can explain why this article was published in such a niche, low-impact, low-prestige journal.
Participants indicated their political (i.e., general), social, and economic orientations on a rating scale from 0 (extremely liberal) to 10 (extremely conservative), with the option to respond with “don't know/prefer not to say.” In addition, participants indicated their attitudes toward 12 social3 (Cronbach's α = 0.83) and economic (Cronbach's α = 0.62) issues (Everett, 2013) by rating how positive or negative they feel about each on a feeling thermometer (0 = negative, 100 = positive). Responses were converted to POMP scores and averaged into two composite variables representing social (social orientation and Everett's social conservatism subscale; Cronbach's α = 0.87) and economic conservatism (economic orientation and Everett's economic conservatism subscale; Cronbach's α = 0.72). The general political orientation question was analyzed separately. In all cases, higher scores indicated greater conservatism.
We used the same religiosity measures as Pennycook et al. (2012). Three religious engagement (Re) questions measured frequency of engaging in religious practices (Cronbach's α = 0.85). Six religious belief (Rb) items measured the extent of belief in religious concepts (Cronbach's α = 0.94). Both scales had a separate “don't know/prefer not to say” response option. All responses were converted to POMP scores and averaged separately. Higher scores indicated higher belief and engagement.
Edited for formatting
"The study examined 426 American adults. Among the sample were 225 Christians, 59 Agnostics, 37 Atheists, 9 Buddhists, 8 Jews, 5 Pagans, 3 Muslims , 30 “others”, and 50 with no affiliation."
Shouldn't the sample size be equally large for each affiliation?
Science AMA Series: Hi this is Robert Morhard, Corrine Nief, Carlos Barrero Castedo and Jenna Mueller at Duke University, we're working on developing an ethanol-based treatment for tumor treatment in resource-limited settings. AUA!
Our recent publication was recently posted here: https://www.reddit.com/sub/science/comments/6xs76y/duke_university_scientists_have_created_a_lethal/.
We've been working on this project for three years now and would love to answer any related questions. This project is a combination of global health and biomedical engineering. We're really excited by our most recent proof-of-concept and are planning more exciting experiments. Feel free to just generally ask about anything biology-related as well.
Answering questions will be:
Robert Morhard, Robert obtained a BS in Biomedical Engineering and Materials Science and Engineering from Carnegie Mellon University in 2012. In 2014 He received an MS in Biomedical Engineering from the Swiss Federal Institute of Technology - Zurich At Duke he works on developing a low-cost ablative tumor therapy for use in resource-limited settings.
Corrine Nief Corrine obtained a BSc in Engineering with minors in Math and Chemistry from Baylor University. She was a summer researcher at Oak Ridge National Lab studying protein structure dynamics with super-computing. Later, she studied mitochondrial protein energetics at The National Institutes of Health. Now at Duke, her research is focused on developing low-cost cancer treatments for cervical and breast cancer.
Carlos Barrero Castedo Undergraduate researcher, Duke University
Jenna MuellerJenna received a B.S. degree in bioengineering with a minor in global health technologies from Rice University, and completed both an M.S. and Ph.D. in biomedical engineering at Duke University. Currently, Jenna is a postdoctoral researcher, who is interested in the intersection of biomedical engineering and global health. Specifically, she is interested in developing low cost optical devices and therapies to diagnose and treat cervical cancer in resource limited settings.
Here is a direct link to our paper: https://www.nature.com/articles/s41598-017-09371-2
Here is a summary of the paper: https://www.acsh.org/news/2017/09/03/ethanol-lethal-injection-tumors-11779
We will be back at 1 pm Et to answer your questions, ask us anything!
In layman's terms how does your treatment work?
What are the side effects?
How will this effect the industry?
How costly will this treatment be?
How long have you worked/been working on developing this treatment?
This is my first question to answer!
-How does this work - We directly inject a solution of ethyl cellulose (similar to the cellulose in plants) in ethanol. Ethyl cellulose is a unique material in that it dissolves in ethanol, but not in water. When you inject the liquid ethyl cellulose-ethanol solution into the water-rich environment of the tumor it undergoes a phase transition and forms a gel. This gel is a similar consistence to wet wood pulp. This is great for treatment because the gel has a very high ethanol concentration and gets retained well inside the tumor. This means that the tumor cells get a longer exposure to ethanol and are more likely to die.
-Side effects: We're not entirely sure. It seems as though there are minimal side effects according to studies done by other groups in the treatment of varicose veins and herniated discs. It'll take some more research to determine if this is true for tumor ablation as well. We hope it is!
-Effect on industry: We'll have to wait to find out!
-Costly: I can only speak to the current cost of the raw materials, and that's very, very cheap.
-Duration of project: About 2.5 years now. It started off with me spending half of my time on it and now it's turning into a pretty large group of brilliant, determined researchers. It's been a fun transition!
How did you get the idea of using ethanol in tumor treatment?
The main challenges are generating the data to assess whether or not this is a safe technique. It's hard to know that until you try it, but you can't try that until you know it. You know?
One of the two drugs used in this study didnt work on guinea pigs back in the day: https://www.ncbi.nlm.nih.gov/m/pubmed/17217163/
No. Mice can have these patches applied and selectively burn regions of adiposity.
"Love handles" is a way of appealing to anyone who might read this.
It's called dinitrophenol and it does exactly that. The side effects are organ failure, over-heating to death, and cataracts. People lose around 2lbs of fat a day on it.
I was very close to using it at one time and even found a reputable supplier (not Chinese stuff) but decided the risks aren't worth it.
Edit: I forgot nerve damage. It actually erodes the Myelin sheath of your nerves causing body wide pain in some people. The halflife is long enough that once you know about the nerve damage it will keep progressing for weeks even if you stop the drug immediately.
If this works in humans they just made a few billion dollars