Scene 1: Two fathers encounter each other at a Boy Scout meeting. After a little conversation, one reveals that his son won’t be playing football because of concerns about head injuries. The other father reveals that he and his son love football, that they spoke with their pediatrician about it, and that their son will continue with football at least into middle school. There’s a bit of wary nodding, and then, back to the Pinewood Derby.
Scene 2: Two mothers meet on a playground. After a little conversation about their toddlers, one mother mentions that she still breastfeeds and practices “attachment parenting,” which is why she has a sling sitting next to her. The other mother mentions that she practiced “cry it out” with her children but that they seem to be doing well and are good sleepers. Then one of the toddlers begins to cry, obviously hurt in some way, and both mothers rush over together to offer assistance.
Scene 3: In the evening, one of these parents might say to a partner, “Can you believe that they’re going to let him play football?” or “I can’t believe they’re still breastfeeding when she’s three!” Sure. They might “judge” or think that’s something that they, as parents, would never do.
But which ones are actually involved in a war?
War. What is it good for?
I can’t answer that question, but I can tell you the definition of ‘war’: “a state of armed conflict between different nations or states or different groups within a nation or state.” Based on this definition and persistent headlines about “Mommy Wars,” you might conclude that a visit to your local playground or a mom’s group outing might require decking yourself out cap-á-pie in Kevlar. But the reality on the ground is different. There is no war. Calling disputes and criticisms and judgments about how other people live “war” is like calling a rowboat on a pond the Titanic. One involves lots of energy release just to navigate relatively placid waters while the other involved a tremendous loss of life in a rough and frigid sea. Big difference.
I’m sure many mothers can attest to the following: You have friends who also are mothers. I bet that for most of us, those friends represent a spectrum of attitudes about parenting, education, religion, Fifty Shades of Grey, recycling, diet, discipline, Oprah, and more. They also probably don’t all dress just like you, talk just like you, have the same level of education as you, same employment, same ambitions, same hair, or same toothpaste. And I bet that for many of us, in our interactions with our friends, we have found ourselves judging everything from why she insists on wearing those shoes to why she lets little Timmy eat Pop Tarts. Yet, despite all of this mental observation and, yes, judging, we still manage to get along, go out to dinner together, meet at one another’s homes, and gab our heads off during play dates.
That’s not a war. That’s life. It’s using our brains as shaped by our cultural understanding and education and rejection or acceptance of things from our own upbringing and talks with medical practitioners and books we’ve read and television shows we’ve watched and, for some of us, Oprah. Not one single friend I have is a cookie cutter representation of me or how I parent. Yet, we are not at war. We are friends. Just because people go online and lay out in black and white the critiques that are in their heads doesn’t mean “war” is afoot. It means expressing the natural human instinct to criticize others in a way that we think argues for Our Way of Doing Things. Online fighting is keeping up with the virtual Joneses. In real life, we are friends with the Joneses, and everyone tacitly understands what’s off limits within the boundaries of that friendship. That’s not war. It’s friendly détente.
The reality doesn’t stop the news media from trying to foment wars, rebellions, and full-on revolutions with provocative online “debates” and, lately, magazine covers. The most recent, from Time, features a slender mother, hand on cocked hip, challenging you with her eyes as she nurses her almost-four-year-old son while he stands on a chair. As Time likely intended, the cover caused an uproar. We’ve lampooned it ourselves (see above).
But the question the cover asks in all caps, “Are you mom enough?” is even more manipulative than the cover because it strikes at the heart of all those unspoken criticisms we think–we know–other women have in their heads about our parenting. What we may not consider is that we, too, are doing the same, and still… we are not actually at war. We’re just women, judging ourselves and other women, just like we’ve done since the dawn of time. It’s called “using your brain.” Inflating our interactions and fairly easily achieved parental philosophy détentes to “war” caricatures us all as shrieking harpies, incapable of backing off and being reasonable.
The real question to ask isn’t “Are you mom enough?” In fact, it’s an empty question because there is no answer. Your parenting may be the most perfect replica of motherhood since the Madonna (the first one), yet you have no idea how that will manifest down the road in terms of who your child is or what your child does. Whether you’re a Grizzly or a Tiger or a Kangaroo or a Panda mother, there is no “enough.”
So, instead of asking you “Are you mom enough?”, in keeping with our goal of bringing women evidence-based science, we’ve looked at some of the research describing what might make a successful parent–child relationship. Yes, the answer is about attachment, but not necessarily of the physical kind. So drop your guilt. Read this when you have time. Meanwhile, do your best to connect with your child, understand your child, and respond appropriately to your child.
Why? Because that is what attachment is–the basic biological response to a child’s needs. If you’re not a nomad or someone constantly on the move, research suggests that the whole “physically attached to me” thing isn’t really a necessary manifestation of attachment. If you harken to it and your child enjoys it (mine did not) and it works for you without seeming like, well, an albatross around your neck, go for it.
What is attachment?
While attachment as a biological norm among primates has been around as long as primates themselves, humans are more complicated than most primates. We have theories. Attachment theory arose from the observations of a couple of human behaviorists or psychologists (depending on whom you ask), John Bowlby and Mary Ainsworth. Bowlby derived the concept of attachment theory, in which an infant homes in on an attachment figure as a “safe place.” The attachment figure, usually a parent, is the person who responds and is sensitive to the infant’s needs and social overtures. That parent is typically the mother, and disruption of this relationship can have, as most of us probably instinctively know, negative effects.
Bowlby’s early approach involved the mother’s having an understanding of the formational experiences of her own childhood and then translating that to an understanding of her child. He even found that when he talked with parents about their own childhoods in front of their children, the result would be clinical breakthroughs for his patients. As he wrote,
Having once been helped to recognize and recapture the feelings which she herself had as a child and to find that they are accepted tolerantly and understandingly, a mother will become increasingly sympathetic and tolerant toward the same things in her child.
Later studies seem to bear out this observation of a connection to one’s childhood experiences and more connected parenting. For example, mothers who are “insightful” about their children, who seek to understand the motivations of their children’s behavior, positively influence both their own sensitivity and the security of their infant’s attachment to them.
While Bowlby’s research focused initially on the effects of absolute separation between mother and child, Mary Ainsworth, an eventual colleague of Bowlby, took these ideas of the need for maternal input a step further. Her work suggested to her that young children live in a world of dual and competing urges: to feel safe and to be independent. An attachment figure, a safe person, is for children an anchor that keeps them from become unmoored even as they explore the unknown waters of life. Without that security backing them up, a child can feel always unmoored and directionless, with no one to trust for security.
Although he was considered an anti-Freudian rebel, Bowlby had a penchant for Freudian language like “superego” and referred to the mother as the “psychic organizer.” Yet his conclusions about the mother–child bond resonate with their plain language:
The infant and young child should experience a warm, intimate, and continuous relationship with his mother (or permanent mother substitute) in which both find satisfaction and enjoyment.
You know, normal biological stuff. As a side note, he was intrigued by the fact that social bonds between mother and offspring in some species weren’t necessarily tied to feeding, an observation worth keeping in mind if you have concerns about not being able to breastfeed.
The big shift here in talking about the mother–child relationship was that Bowlby was proposing that this connection wasn’t some Freudian libidinous communion between mother and child but instead a healthy foundation of a trust relationship that could healthily continue into the child’s adulthood.
Ainsworth carried these ideas to specifics, noting in the course of her observations of various groups how valuable a mother’s sensitivity to her child’s behaviors were in establishing attachment. In her most famous study, the “Baltimore study” [PDF], she monitored 26 families with new babies. She found that “maternal responsiveness” in the context of crying, feeding, playing, and reciprocating seemed to have a powerful influence on how much a baby cried in later months, although some later studies dispute specific influences on crying frequencies.
Ainsworth also introduced the “Strange Situation” lab test, which seems to have freaked people out when it first entered the research scene. In this test, over the course of 20 minutes, a one-year-old baby is in a room full toys, first with its mother, then with mother and a strange woman, then with the stranger only (briefly), then with the mother, and then alone before the stranger and then the mother return. The most interesting findings of the study came from when the mother returned after her first absence, having left the baby alone in the room with a stranger. Some babies seemed quite angry, wanting to be with their mothers but expressing unhappiness with her at the same time and physically rejecting her.
From her observations during the Strange Situation, Ainsworth identified three types of attachment. The first was “Secure,” which, as its name implies, suggested an infant secure and comfortable with an attachment figure, a person with whom the infant actively seeks to interact. Then there’s the insecure–avoidant attachment type, in which an infant clearly is not interested in being near or interacting with the attachment figure. Most complex seems to be the insecure–resistant type, and the ambivalence of the term reflects the disconnected behavior the infant shows, seeming to want to be near the attachment figure but also resisting, as some of the unhappy infants described above behaved in the Strange Situation.
Within these types are now embedded various subtypes, including a disorganized–disoriented type in which the infant shows “odd” and chaotic behavior that seems to have no distinct pattern related to the attachment figure.
As you read this, you may be wondering, “What kind of attachment do my child and I have?” If you’re sciencey, you may fleetingly even have pondered conducting your own Strange Situation en famille to see what your child does. I understand the impulse. But let’s read on.
What are the benefits of attachment?
Mothers who are sensitive to their children’s cues and respond in ways that are mutually satisfactory to both parties may be doing their children a lifetime of favors, in addition to the parental benefit of a possibly less-likely-to-cry child. For example, a study of almost 1300 families looked at levels of cortisol, the “stress” hormone, in six-month-old infants and its association with maternal sensitivity to cues and found lower levels in infants who had “more sensitive” mothers.
Our understanding of attachment and its importance to infant development can help in other contexts. We can apply this understanding to, for example, help adolescent mothers establish the “secure” level of attachment with their infants. It’s also possibly useful in helping women who are battling substance abuse to still establish a secure attachment with their children.
On a more individual level, it might help in other ways. For example, if you want your child to show less resistance during “clean-up” activities, establishing “secure attachment” may be your ticket to a better-looking playroom.
More seriously, another study has found that even the way a mother applies sensitivity can be relevant. Using the beautiful-if-technical term ‘dyads’ to refer to the mother–child pair, this study included maternal reports of infant temperament and observations of maternal sensitivity to both infant distress and “non-distress.” Further, the authors assessed the children behaviorally at ages 24 and 36 months for social competence, behavioral problems, and typicality of emotional expression. They found that a mother’s sensitivity to an infant’s distress behaviors was linked to fewer behavioral problems and greater social competence in toddlerhood. Even more intriguing, the child’s temperament played a role: for “temperamentally reactive” infants, a mother’s sensitivity to distress was linked to less dysregulation of the child’s emotional expression in toddlerhood.
And that takes me to the child, the partner in the “dyad”
You’re not the only person involved in attachment. As these studies frequently note, you are involved in a “dyad.” The other member of that dyad is the child. As much as we’d like to think that we can lock down various aspects of temperament or expression simply by forcing it with our totally excellent attachment skills, the child in your dyad is a person, too, who arrived with a bit of baggage of her own.
And like the study described above, the child’s temperament is a key player in the outcome of the attachment tango. Another study noted that multiple factors influence “attachment quality.” Yes, maternal sensitivity is one, but a child’s native coping behaviors and temperament also seem to be involved. So, there you have it. If you’re feeling like a parental failure, science suggests you can quietly lay at least some of the blame on the Other in your dyad–your child. Or, you could acknowledge that we’re all human and this is just part of our learning experience together.
What does attachment look like, anyway?
Dr. William Sears took the concept of attachment and its association with maternal sensitivity to a child’s cues and security and… wrote a book that literally translated attachment as a physical as well as emotional connection. This extension of attachment–which Sears appends to every aspect of parenting, from pregnancy to feeding to sleeping–has become in the minds of some parents a prescriptive way of doing things with benefits that exclude all other parenting approaches or “philosophies.” It also involves the concept of “baby wearing,” which always brings up strange images in my mind and certainly takes outré fashion to a whole new level. In reality, it’s just a way people have carried babies for a long time in the absence of other easy modes of transport.
When I was pregnant with our first child and still blissfully ignorant about how little control parents have over anything, I read Sears’ book about attachment parenting. Some of it is common-sense, broadly applicable parenting advice: respond to your child’s needs. Some of it is simply downright impossible for some parent–child dyads, and much of it is based on the presumption that human infants in general will benefit from a one-size-fits-all sling of attachment parenting, although interpretations of the starry-eyed faithful emphasize that more than Sears does.
Because much of what Sears wrote resonated with me, we did some chimeric version of attachment parenting–or, we tried. The thing is, as I noted above, the infant has some say in these things as well. Our oldest child, who is autistic, was highly resistant to being physically attached much of the time. He didn’t want to sleep with us past age four months, and he showed little interest in aspects of attachment parenting like “nurturing touch,” which to him was seemingly more akin to “taser touch.” We ultimately had three sons, and in the end, they all preferred to sleep alone, each at an earlier and earlier age. The first two self-weaned before age one because apparently, the distractions of the sensory world around them were far more interesting than the same boring old boob they kept seeing immediately in front of their faces. Our third was unable to breastfeed at all.
So, like all parents do, we punted, in spite of our best laid plans and intentions. Our hybrid of “attachment parenting” could better be translated into “sensitivity parenting,” because our primary focus, as we punted and punted and punted our way through the years, was shifting our responses based on what our children seemed to need and what motivated their behaviors. Thus, while our oldest declined to sleep with us according to the attachment parenting commandment, he got to sleep with a boiled egg because that’s what he wanted. Try to beat that, folks, and sure, bring on the judging.
The Double X Science Sensitivity Parenting (TM) cheat sheet.
What does “sensitive” mean?
And finally, the nitty-gritty bullet list you’ve been waiting for. If attachment doesn’t mean slinging your child to your body until you’re lumbar gives out or the child receives a high-school diploma, and parenting is, indeed, one compromise after another based on the exigencies of the moment, what consistent tenets can you practice that meet the now 60-year-old concept of “secure” attachment between mother and child, father and child, or mother or father figure and child? We are Double X Science, here to bring you evidence-based information, and that means lists. The below list is an aggregate of various research findings we’ve identified that seem reasonable and reasonably supported. We’ve also provided our usual handy quick guide for parents in a hurry.
Plan ahead. We know that life is what happens while you’re planning things, but… life does happen, and plans can at least serve as a loose guide to navigation. So, plan that you will be a parent who is sensitive to your child’s needs and will work to recognize them.
Practice emotion detection. Work on that. It doesn’t come easily to everyone because the past is prologue to what we’re capable of in the present. Ask yourself deliberately what your child’s emotion is communicating because behavior is communication. Be the grownup, even if sometimes, the wailing makes you want your mommy. As one study I found notes, “Crying is an aversive behavior.” Yes, maybe it makes you want to cover your ears and run away screaming. But you’re the grownup with the analytical tools at hand to ask “Why” and seek the answer.
Have infant-oriented goals. If you tend to orient your goals in your parent–child dyad toward a child-related benefit (relieve distress) rather than toward a parent-oriented goal (fitting your schedule in some way), research suggests that your dyad will be a much calmer and better mutually adapted dyad.
Trust yourself and keep trying. If your efforts to read your child’s feelings or respond to your child’s needs don’t work right away, don’t give up, don’t read Time magazine covers, and don’t listen to that little voice in your head saying you’re a bad parent or the voice in other people’s heads screaming that at you. Just keep trying. It’s all any of us can do, and we’re all going to screw this up here and there.
Practice behaviors that are supportive of an infant’s sensory needs. For example, positive inputs like a warm voice and smiling are considered more effective than a harsh voice or being physically intrusive. Put yourself in your child’s place and ask, How would that feel? That’s called empathy.
Engage in reciprocation. Imitating back your infant’s voice or faces, or showing joint attention–all forms of joint engagement–are ways of telling an infant or young child that yes, you are the anchor here, the one to trust, and really good time, to boot. Allowing this type of attention to persist as long as the infant chooses rather than shifting away from it quickly is associated with making the child comfortable with independence and learning to regulate behaviors.
Talk to your child. We are generally a chatty species, but we also need to learn to chat. “Rich language input” is important in early child development beginning with that early imitation of your infant’s vocalizations.
Lather, rinse, repeat, adjusting dosage as necessary based on age, weight, developmental status, nanosecond-rate changes in family dynamics and emotional conditions, the teen years, and whether or not you have access to chocolate. See? This stuff is easy.
As you read these lists and about research on attachment, you’ll see words like “secure” and “warm” and “intimate” and “safe.” Are you doing this for your child or doing your best to do it? Then you are, indeed, mom enough, whether you wear your baby or those shoes or both. That doesn’t mean that when you tell other women the specifics of your parenting tactics, they won’t secretly be criticizing you. Sure, we’ll all do that. And then a toddler will cry, we’ll drop it, and move on to mutually compatible things.
Yes, if we’re being honest, it makes most of us feel better to think that somehow, in some way, we’re kicking someone else’s ass in the parenting department. Unfortunately for that lowly human instinct, we’re all parenting unique individuals, and while we may indeed kick ass uniquely for them, our techniques simply won’t extend to all other children. It’s not a war. It’s human… humans raising other humans. Not one thing we do, one philosophy we follow, will guarantee the outcome we intend. We don’t even need science, for once, to tell us that.
According to Leslie Brunetta, she now has much more hair than she had last July.
We became aware of Leslie Brunetta because of her book, Spider Silk: Evolution and 400 Million Years of Spinning, Waiting, Snagging, and Mating, co-authored with Catherine L. Craig. Thanks to a piece Leslie wrote for the Concord Monitor (and excerpted here), we also learned that she is a breast cancer survivor. Leslie agreed to an interview about her experience, and in her emailed responses, she candidly talks about her diagnosis, treatment, and follow-up for her cancers, plural: She was diagnosed simultaneously with two types of breast cancer.
DXS: In your Concord Monitor piece, you describe the link between an understanding of the way evolution happens and some of the advances in modern medicine. What led you to grasp the link between the two?
LB: I think, because I’m not a scientist (I’m an English major), a lot of things that scientists think are obvious strike me as revelations. I somehow had never realized that the search for what would turn out to be DNA began with trying to explain how, in line with the theory of evolution by natural selection, variation arises and traits are passed from generation to generation. As I was figuring out what each chapter in Spider Silk would be about, I tried to think about the questions non-biologists like me would still have about evolution when they got to that point in the book. By the time we got past dragline silk, I realized that we had so far fleshed out the ways that silk proteins could and have evolved at the genetic level. But that explanation probably wouldn’t answer readers’ questions about how, for example, abdominal spinnerets—which are unique to spiders—might have evolved: the evolution of silk is easier to untangle than the evolution of body parts, which is why we focused on it in the first place.
I decided I wanted to write a chapter on “evo-devo,” evolutionary developmental biology, partly because there was a cool genetic study on the development of spinnerets that showed they’ve evolved from limbs. Fortunately, my co-author, Cay Craig, and editor at Yale, Jean Thomson Black, okayed the idea, because that chapter wasn’t in the original proposal. Writing that chapter, I learned why it took so long—nearly a century—to get from Darwin and Mendel to Watson and Crick and then so long again to get to where we are today. If we non-scientists understand something scientific, it’s often how it works, not how a whole string of people over the course of decades building on each other’s work discovered how it works. I knew evolution was the accumulation of gene changes, but, until I wrote that chapter, it hadn’t occurred to me that people began to look for genes because they wanted to understand evolution.
So that was all in the spider part of my life. Then, a few months into the cancer part of my life, I was offered a test called Oncotype DX, which would look at genetic markers in my tumor cells to develop a risk profile that could help me decide whether I should have chemotherapy plus tamoxifen or just tamoxifen. The results turned out to be moot in my case because I had a number of positive lymph nodes, although it was reassuring to find out that the cancer was considered low risk for recurrence. But still—the idea that a genetic test could let some women avoid chemo without taking on extra risk, that’s huge. No one would want to go through chemo if it wasn’t necessary. So by then I was thinking, “Thank you, Darwin!”
And then, coincidentally, the presidential primary season was heating up, and there were a number of serious candidates (well, serious in the sense that they had enough backing to get into the debates) who proudly declared that they had no time for the theory of evolution. And year after year these stupid anti-evolution bills are introduced in various state legislatures. While I was lying on the couch hanging out in the days after chemo sessions, I started thinking, “So, given that you don’t give any credence to Darwin and his ideas, would you refuse on principle to take the Oncotype test or gene-based therapies like Gleevec or Herceptin if you had cancer or if someone in your family had cancer? Somehow I don’t think so.” That argument is not going to convince hard-core denialists (nothing will), but maybe the cognitive dissonance in connection with something as concrete as cancer will make some people who waver want to find out more.
DXS: You mention having been diagnosed with two different forms of cancer, one in each breast. Can you say what each kind was and, if possible, how they differed?
LB: Yes, I unfortunately turned out to be an “interesting” case. This is one arena where, if you possibly can, you want to avoid being interesting. At first it seemed that I had a tiny lesion that was an invasive ductal carcinoma (IDC) and that I would “just” need a lumpectomy and radiation. Luckily for me, the doctor reading my mammogram is known as an eagle eye, and she saw a few things that—given the positive finding from the biopsy—concerned her. She recommended an MRI. In fact, even though I switched to another hospital for my surgery, she sent emails there saying I should have an MRI. That turned up “concerning” spots in both breasts, which led to more biopsies, which revealed multiple tiny cancerous lesions. The only reasonable option was then a double mastectomy.
The lesions in the right breast were IDCs. About 70% of breast cancers are diagnosed as IDCs. Those cancers start with the cells lining the milk ducts. The ones in the left breast were invasive lobular carcinomas (ILCs), which start in the lobules at the end of the milk ducts. Only about 10% of breast cancers are ILCs.
Oncologists hate lobular cancer. Unlike ductal cancers, which form as clumps of cells, lobular cancers form as single-file ribbons of cells. The tissue around ductal cancer cells reacts to those cells, which is why someone may feel a lump—she’s (or he’s) not feeling the cancer itself but the inflammation of the tissue around it. And because the cells clump, they show up more readily on mammograms. Not so lobular cancers. They mostly don’t give rise to lumps and they’re hard to spot on mammograms. They snake their way through tissue for quite a while without bothering anything.
In my case, this explains why last spring felt like an unremitting downhill slide. Every time someone looked deeper, they found something worse. It turned out that on my left side, the lobular side, I had multiple positive lymph nodes, which was why I needed not just chemo but also radiation (which usually isn’t given after a mastectomy). That was the side that didn’t even show up much on the mammogram. On the right side, the ductal side, which provoked the initial suspicions, my nodes were clear. I want to write about this soon, because I want to find out more about it. I’ve only recently gotten to the place emotionally where I think I can deal with reading the research papers as opposed to more general information. By the way, the resource that most helped us better understand what my doctors were talking about was Dr. Susan Love’s Breast Book. It was invaluable as we made our way through this process, although it turned out that I had very few decisions to make because there was usually only one good option.
DXS: As part of your treatment, you had a double mastectomy. One of our goals with this interview is to tell women what some of these experiences with treatment are like. If you’re comfortable doing so, could you tell us a little bit about what a double mastectomy entails and what you do after one in practical terms?
LB: A mastectomy is a strange operation. In a way, it’s more of an emotional and psychological experience than a physical experience. My surgeon, who was fantastic, is a man, and when we discussed the need for the mastectomies he said that I would be surprised at how little pain would be involved and how quick the healing would be. Even though I trusted him a lot by then, my reaction was pretty much, “Like you would know, right?” But he did know. When you think about it, it’s fairly non-invasive surgery. Unless the cancer has spread to the surrounding area, which doesn’t happen very often now due to early detection, no muscle or bone is removed. (Until relatively recently, surgeons removed the major muscle in the chest wall, and sometimes even bone, because they believed it would cut the risk of recurrence. That meant that many women lost function in their arm and also experienced back problems.) None of your organs are touched. They don’t go into your abdominal cavity. Also, until recently, they removed a whole clump of underarm lymph nodes when they did lumpectomies or mastectomies. Now they usually remove just a “sentinel node,” because they know that it will give them a fairly reliable indicator of whether the cancer has spread to the other nodes. That also makes the surgery less traumatic than it used to be.
I opted not to have reconstruction. Reconstruction is a good choice for many women, but I didn’t see many benefits for me and I didn’t like the idea of a more complicated surgery. My surgery was only about two hours. I don’t remember any pain at all afterwards, and my husband says I never complained of any. I was in the hospital for just one night. By the next day, I was on ibuprofen only. The bandages came off two days after the surgery.
That’s shocking, to see your breasts gone and replaced by thin red lines, no matter how well you’ve prepared yourself. It made the cancer seem much more real in some way than it had seemed before. In comparison, the physical recovery from the surgery was fairly minor because I had no infections or complications. There were drains in place for about 10 days to collect serum, which would otherwise collect under the skin, and my husband dealt with emptying them twice a day and measuring the amount. I had to sleep on my back, propped up, because of where the drains were placed, high up on my sides, and I never really got used to that. It was a real relief to have the drains removed.
My surgeon told me to start doing stretching exercises with my arms right away, and that’s really important. I got my full range of motion back within a couple of months. But even though I had my surgery last March, I’ve noticed lately that if I don’t stretch fully, like in yoga, things tighten up. That may be because of the radiation, though, because it’s only on my left side. Things are never quite the same as they were before the surgery, though. Because I did have to have the axillary nodes out on my left side, my lymph system is disrupted. I haven’t had any real problems with lymphedema yet, and I may never, but in the early months I noticed that my hands would swell if I’d been walking around a lot, and I’d have to elevate them to get them to drain back. That rarely happens now. But I’ve been told I need to wear a compression sleeve if I fly because the change in air pressure can cause lymph to collect. Also, I’m supposed to protect my hands and arms from cuts as much as possible. It seems to me that small nicks on my fingers take longer to heal than they used to. So even though most of the time it seems like it’s all over, I guess in those purely mechanical ways it’s never over. It’s not just that you no longer have breasts, it’s also that nerves and lymph channels and bits of tissue are also missing or moved around.
The bigger question is how one deals with now lacking breasts. I’ve decided not to wear prostheses. I can get away with it because I was small breasted, I dress in relatively loose clothes anyway, and I’ve gained confidence over time that no one notices or cares and I care less now if they do notice. But getting that self-confidence took quite a while. Obviously, it has an effect on my sex life, but we have a strong bond and it’s just become a piece of that bond. The biggest thing is that it’s always a bit of a shock when I catch sight of myself naked in a mirror because it’s a reminder that I’ve had cancer and there’s no getting around the fact that that sucks.
DXS: My mother-in-law completed radiation and chemo for breast cancer last year, and if I remember correctly, she had to go frequently for a period of weeks for radiation. Was that you experience? Can you describe for our readers what the time investment was like and what the process was like?
LB: I went for radiation 5 days a week for about 7 weeks. Three days a week, I’d usually be in and out of the hospital within 45 minutes. One day a week, I met with the radiology oncologist and a nurse to debrief, which was also a form of emotional therapy for me. And one day a week, they laid on a chair massage, and the nurse/massage therapist who gave the massage was great to talk to, so that was more therapy. Radiation was easy compared to chemo. Some people experience skin burning and fatigue, but I was lucky that I didn’t experience either. Because I’m a freelancer, the time investment wasn’t a burden for me. I’m also lucky living where I live, because I could walk to the hospital. It was a pleasant 3-mile round-trip walk, and I think the walking helped me a lot physically and mentally.
DXS: And now to the chemo. My interest in interviewing you about your experience began with a reference you made on Twitter to “chemo brain,” and of course, after reading your evolution-medical advances piece. Can you tell us a little about what the process of receiving chemotherapy is like? How long does it take? How frequently (I know this varies, but your experience)?
LB: Because of my age (I was considered young, which was always nice to hear) and state of general good health, my oncologist put me on a dose-dense AC-T schedule. This meant going for treatment every two weeks over the course of 16 weeks—8 treatment sessions. At the first 4 sessions, I was given Adriamycin and Cytoxan(AC), and the last 4 sessions I was given Taxol (T). The idea behind giving multiple drugs and giving them frequently is that they all attack cancer cells in different ways and—it goes back to evolution—by attacking them frequently and hard on different fronts, you’re trying to avoid selecting for a population that’s resistant to one or more of the drugs. They can give the drugs every two weeks to a lot of patients now because they’ve got drugs to boost the production of white blood cells, which the cancer drugs suppress. After most chemo sessions, I went back the next day for a shot of one of these drugs, Neulasta.
The chemo clinic was, bizarrely, a very relaxing place. The nurses who work there were fantastic, and the nurse assigned to me, Kathy, was always interesting to talk with. She had a great sense of humor, and she was also interested in the science behind everything we were doing, so if I ever had questions she didn’t have ready answers for, she’d find out for me. A lot of patients were there at the same time, but we each had a private space. You’d sit in a big reclining chair. They had TVs and DVDs, but I usually used it as an opportunity to read. My husband sat through the first session with me, and a close friend who had chemo for breast cancer 15 years ago sat through a few other sessions, but once I got used to it, I was comfortable being there alone. Because of the nurses, it never felt lonely.
I’d arrive and settle in. Kathy would take blood for testing red and white blood counts and, I think, liver function and some other things, and she’d insert a needle and start a saline drip while we waited for the results. I’ve always had large veins, so I opted to have the drugs administered through my arm rather than having a port implanted in my chest. Over the course of three to four hours, she’d change the IV bags. Some of the bags were drugs to protect against nausea, so I’d start to feel kind of fuzzy—I don’t think I retained a whole lot of what I read there! The Adriamycin was bright orange; they call it the Red Devil, because it can chew up your veins—sometimes it felt like it was burning but Kathy could stop that by slowing the drip. Otherwise, it was fairly uneventful. I’d have snacks and usually ate lunch while still hooked up.
I was lucky I never had any reactions to any of the drugs, so actually getting the chemo was a surprisingly pleasant experience just because of the atmosphere. On the one hand, you’re aware of all these people around you struggling with cancer and you know things aren’t going well for some of them, so it’s heartbreaking, and also makes you consider, sometimes fearfully, your own future no matter how well you’re trying to brace yourself up. But at the same time, the people working there are so positive, but not in a Pollyannaish-false way, that they helped me as I tried to stay positive. The social worker stopped in with each patient every session, and she was fantastic—I could talk out any problems or fears I had with her, and that helped a huge amount.
DXS: Would you be able to run us through a timeline of the physical effects of chemotherapy after an infusion? How long does it take before it hits hardest? My mother-in-law told me that her biggest craving, when she could eat, was for carb-heavy foods like mashed potatoes and for soups, like vegetable soup. What was your experience with that?
LB: My biggest fear when I first learned I would need chemo was nausea. My oncologist told us that they had nausea so well controlled that over the past few years, she had only had one or two patients who had experienced it. As with the surgeon’s prediction about mastectomy pain, this turned out to be true: I never had even a single moment of nausea.
But there were all sorts of other effects. For the first few days after a session, the most salient effects were actually from the mix of drugs I took to stave off nausea. I generally felt pretty fuzzy, but not necessarily sleepy—part of the mix was steroids, so you’re a little hyped. There’s no way I’d feel safe driving on those days, for example. I’d sleep well the first three nights because I took Ativan, which has an anti-nausea effect. But except for those days, my sleep was really disrupted. Partly that’s because, I’m guessing, the chemo hits certain cells in your brain and partly it’s because you get thrown into chemical menopause, so there were a lot of night hot flashes. Even though I’d already started into menopause, this chemo menopause was a lot more intense and included all the symptoms regularly associated with menopause.
By the end of the first session, I was feeling pretty joyful because it was much less bad than I had thought it would be. By the second week in the two-week cycle, I felt relatively normal. But even though it never got awful, the effects started to accumulate. My hair started to fall out the morning I was going to an award ceremony for Spider Silk. It was ok at the ceremony, but we shaved it off that night. I decided not to wear a wig. First, it was the summer, and it would have been hot. Second, I usually have close to a buzz cut, and I can’t imagine anyone would make a wig that would look anything like my hair. My kids’ attitude was that everyone would know something was wrong anyway, so I should just be bald, and that helped a lot. But it’s hard to see in people’s eyes multiple times a day their realization that you’re in a pretty bad place. Also, it’s not just your head hair that goes. So do your eyebrows, your eyelashes, your pubic hair, and most of the tiny hairs all over your skin. And as your skin cells are affected by the chemo (the chemo hits all fast-reproducing cells), your skin itself gets more sensitive and then is not protected by those tiny hairs. I remember a lot of itching. And strange things like my head sticking to my yoga mat and my reading glasses sticking to the side of my head instead of sliding over my ears.
I never lost my appetite, but I did have food cravings during the AC cycles. I wanted sushi and seaweed salad, of all things. And steak. My sense of taste went dull, so I also wanted things that tasted strong and had crunch. I stopped drinking coffee and alcohol, partly because of the sleep issues but partly because it didn’t taste very good anyway. I drank loads of water on the advice of the oncologist, the nurses, and my acupuncturist, and I think that helped a lot.
During the second cycle, I developed a fever. That was scary. I was warned that if I ever developed a fever, I should call the oncologist immediately, no matter the time of day or day of week. The problem is that your immune response is knocked down by the chemo, so what would normally be a small bacterial infection has the potential to rage out of control. I was lucky. We figured out that the source of infection was a hemorrhoid—the Adriamycin was beginning to chew into my digestive tract, a well-known side effect. (Having to pay constant attention to yet another usually private part of the body just seemed totally unfair by this point.) Oral antibiotics took care of it, which was great because I avoided having to go into the hospital and all the risks entailed with getting heavy-duty IV antibiotic treatment. And we were also able to keep on schedule with the chemo regimen, which is what you hope for.
After that, I became even more careful about avoiding infection, so I avoided public places even more than I had been. I’m very close to a couple of toddlers, and I couldn’t see them for weeks because they were in one of those toddler constant-viral stages, and I really missed them.
The Taxol seems to be much less harsh than the AC regimen, so a lot of these side effects started to ease off a bit by the second 8 weeks, which was certainly a relief.
I was lucky that I didn’t really have mouth sores or some of the other side effects. Some of this is, I think, just because besides the cancer I don’t have any other health issues. Some of it is because my husband took over everything and I don’t have a regular job, so I had the luxury of concentrating on doing what my body needed. I tried to walk every day, and I slept when I needed to, ate when and what I needed to, and went to yoga class when my immune system was ok. I also went to acupuncture every week. I know the science is iffy on that, but I think it helped me with the side effects, even if it was the placebo effect at work (I’m a big fan of the placebo effect). We also both had extraordinary emotional support from many friends and knew we could call lots of people if we needed anything. That’s huge when you’re in this kind of situation.
Currently, I’m still dealing with some minor joint pains, mostly in my wrists and feet. I wasn’t expecting this problem, but my oncologist says it’s not uncommon: they think it’s because your immune system has to re-find its proper level of function, and it can go into overdrive and set up inflammation in the joints. That’s gradually easing off, though.
Most people don’t have it as easy as I did in terms of the medical, financial, and emotional resources I had to draw on. I’m very mindful of that and very grateful.
DXS: You say that you had “few terrible side effects” and a “very cushy home situation.” I’m sure any woman would like to at least be able to experience the latter while dealing with a full-body chemical attack. What were some factors that made it “cushy” that women might be able to talk to their families or caregivers about replicating for them?
LB: As I’ve said, some of it is just circumstance. For example, my kids were old enough to be pretty self-sufficient and old enough to understand what was going on, which meant both that they needed very little from me in terms of care and also that they were less scared than they might have been if they were younger. My husband happens to be both very competent (more competent than I am) around the house and very giving. I live in Cambridge, MA, where I could actually make choices about where I wanted to be treated at each phase and know I’d get excellent, humane care and where none of the facilities I went to was more than about 20 minutes away.
Some things that women might have some control over and that their families might help nudge them toward:
Find doctors you trust. Ask a lot of questions and make sure you understand the answers. But don’t get hung up on survival or recurrence statistics. There’s no way to know for sure what your individual outcome will be. Go for the treatment that you and your doctors believe will give you the best chance, and then assume as much as possible that your outcome will be good.
Make sure you talk regularly with a social worker or other therapist who specializes in dealing with breast cancer patients. If you have fears or worries that you don’t want to talk to your partner or family about, here’s where you’ll get lots of help.
Find compatible friends who have also had cancer to talk to. I had friends who showed me their mastectomy scars, who showed me their reconstructions, who told me about their experiences with chemo and radiation, who told me about what life after treatment was like (is still like decades later…). And none of them told me, “You should…” They all just told me what was hard for them and what worked for them and let me figure out what worked for me. Brilliant.
Try to get some exercise even if you don’t feel like it. It was often when I felt least like moving around that a short walk made me feel remarkably better. But I would forget that, so my husband would remind me. Ask someone to walk with you if you’re feeling weak. Getting your circulation going seems to help the body process the chemo drugs and the waste products they create. For the same reason, drink lots of water.
Watch funny movies together. Laughter makes a huge difference.
Pamper yourself as much as possible. Let people take care of you and help as much as they’re willing. But don’t be afraid to say no to anything that you don’t want or that’s too much.
Family members and caregivers should also take care of themselves by making some time for themselves and talking to social workers or therapists if they feel the need. It’s a big, awful string of events for everyone involved, not just the patient.
DXS: In the midst of all of this, you seem to have written a fascinating book about spiders and their webs. Were you able to work while undergoing your treatments? Were there times that were better than others for attending to work? Could work be a sort of occupational therapy, when it was possible for you to do it, to keep you engaged?
LB: The book had been published about 6 months before my diagnosis. The whole cancer thing really interfered not with the writing, but with my efforts to publicize it. I had started to build toward a series of readings and had to abandon that effort. I had also started a proposal for a new book and had to put that aside. I had one radio interview in the middle of chemo, which was kind of daunting but I knew I couldn’t pass up the opportunity, and when I listen to it now, I can hear my voice sounds kind of shaky. It went well, but I was exhausted afterwards. Also invigorated, though—it made me feel like I hadn’t disappeared into the cancer. I had two streams of writing going on, both of which were therapeutic. I sent email updates about the cancer treatment to a group of friends—that was definitely psychological therapy. I also tried to keep the Spider Silk blog up to date by summarizing related research papers and other spider silk news—that was intellectual therapy. I just worked on them when I felt I wanted to. The second week of every cycle my head was usually reasonably clear.
I don’t really know whether I have chemo brain. I notice a lot of names-and-other-proper-nouns drop. But whether that’s from the chemo per se, or from the hormone changes associated with the chemically induced menopause, or just from emotional overload and intellectual distraction, I don’t know. I find that I’m thinking more clearly week by week.
DXS: What is the plan for your continued follow-up? How long will it last, what is the frequency of visits, sorts of tests, etc.?
LB: I’m on tamoxifen and I’ll be on that for probably two years and then either stay on that or go onto an aromatase inhibitor [Ed. note: these drugs block production of estrogen and are used for estrogen-sensitive cancers.] for another three years. I’ll see one of the cancer doctors every three months for at least a year, I think. They’ll ask me questions and do a physical exam and take blood samples to test for tumor markers. At some point the visits go to every six months.
For self-care, I’m exercising more, trying to lose some weight, and eating even better than I was before.
DXS: Last…if you’re comfortable detailing it…what led to your diagnosis in the first place?
LB: My breast cancer was uncovered by my annual mammogram. I’ve worried about cancer, as I suppose most people do. But I never really worried about breast cancer. My mother has 10 sisters and neither she nor any of them ever had breast cancer. I have about 20 older female cousins—I was 50 when I was diagnosed last year–and as far as I know none of them have had breast cancer. I took birth control pills for less than a year decades ago. Never smoked. Light drinker. Not overweight. Light exerciser. I breastfed both kids, although not for a full year. Never took replacement hormones. Never worked in a dangerous environment. Never had suspicious mammograms before. So on paper, I was at very low risk as far as I can figure out. After I finished intensive treatment, I was tested for BRCA1 and BRCA2 (because mutations there are associated with cancer in both breasts) and no mutations were found. Unless or until some new genetic markers are found and one of them applies to me, I think we’ll never know why I got breast cancer, other than the fact that I’ve lived long enough to get cancer. There was no lump. Even between the suspicious mammogram and ultrasound and the biopsy, none of the doctors examining me could feel a lump or anything irregular. It was a year ago this week that I got the news that the first biopsy was positive. In some ways, because I feel really good now, it’s hard to believe that this year ever happened. But in other ways, the shock of it is still with me and with the whole family. Things are good for now, though, and although I feel very unlucky that this happened in the first place, I feel extremely lucky with the medical care I received and the support I got from family and friends and especially my husband.
Leslie Brunetta’s articles and essays have appeared in the New York Times,Technology Review, and the Sewanee Review as well as on NPR and elsewhere. She is co-author, with Catherine L. Craig, of Spider Silk: Evolution and 400 Million Years of Spinning, Waiting, Snagging, and Mating (Yale University Press).
The four basic categories of molecules for building life are carbohydrates, lipids, proteins, and nucleic acids.
Carbohydrates serve many purposes, from energy to structure to chemical communication, as monomers or polymers.
Lipids, which are hydrophobic, also have different purposes, including energy storage, structure, and signaling.
Proteins, made of amino acids in up to four structural levels, are involved in just about every process of life.
The nucleic acids DNA and RNA consist of four nucleotide building blocks, and each has different purposes.
The longer version
Life is so diverse and unwieldy, it may surprise you to learn that we can break it down into four basic categories of molecules. Possibly even more implausible is the fact that two of these categories of large molecules themselves break down into a surprisingly small number of building blocks. The proteins that make up all of the living things on this planet and ensure their appropriate structure and smooth function consist of only 20 different kinds of building blocks. Nucleic acids, specifically DNA, are even more basic: only four different kinds of molecules provide the materials to build the countless different genetic codes that translate into all the different walking, swimming, crawling, oozing, and/or photosynthesizing organisms that populate the third rock from the Sun.
Big Molecules with Small Building Blocks
The functional groups, assembled into building blocks on backbones of carbon atoms, can be bonded together to yield large molecules that we classify into four basic categories. These molecules, in many different permutations, are the basis for the diversity that we see among living things. They can consist of thousands of atoms, but only a handful of different kinds of atoms form them. It’s like building apartment buildings using a small selection of different materials: bricks, mortar, iron, glass, and wood. Arranged in different ways, these few materials can yield a huge variety of structures.
We encountered functional groups and the SPHONC in Chapter 3. These components form the four categories of molecules of life. These Big Four biological molecules are carbohydrates, lipids, proteins, and nucleic acids. They can have many roles, from giving an organism structure to being involved in one of the millions of processes of living. Let’s meet each category individually and discover the basic roles of each in the structure and function of life.
You have met carbohydrates before, whether you know it or not. We refer to them casually as “sugars,” molecules made of carbon, hydrogen, and oxygen. A sugar molecule has a carbon backbone, usually five or six carbons in the ones we’ll discuss here, but it can be as few as three. Sugar molecules can link together in pairs or in chains or branching “trees,” either for structure or energy storage.
When you look on a nutrition label, you’ll see reference to “sugars.” That term includes carbohydrates that provide energy, which we get from breaking the chemical bonds in a sugar called glucose. The “sugars” on a nutrition label also include those that give structure to a plant, which we call fiber. Both are important nutrients for people.
Sugars serve many purposes. They give crunch to the cell walls of a plant or the exoskeleton of a beetle and chemical energy to the marathon runner. When attached to other molecules, like proteins or fats, they aid in communication between cells. But before we get any further into their uses, let’s talk structure.
The sugars we encounter most in basic biology have their five or six carbons linked together in a ring. There’s no need to dive deep into organic chemistry, but there are a couple of essential things to know to interpret the standard representations of these molecules.
Check out the sugars depicted in the figure. The top-left molecule, glucose, has six carbons, which have been numbered. The sugar to its right is the same glucose, with all but one “C” removed. The other five carbons are still there but are inferred using the conventions of organic chemistry: Anywhere there is a corner, there’s a carbon unless otherwise indicated. It might be a good exercise for you to add in a “C” over each corner so that you gain a good understanding of this convention. You should end up adding in five carbon symbols; the sixth is already given because that is conventionally included when it occurs outside of the ring.
On the left is a glucose with all of its carbons indicated. They’re also numbered, which is important to understand now for information that comes later. On the right is the same molecule, glucose, without the carbons indicated (except for the sixth one). Wherever there is a corner, there is a carbon, unless otherwise indicated (as with the oxygen). On the bottom left is ribose, the sugar found in RNA. The sugar on the bottom right is deoxyribose. Note that at carbon 2 (*), the ribose and deoxyribose differ by a single oxygen.
The lower left sugar in the figure is a ribose. In this depiction, the carbons, except the one outside of the ring, have not been drawn in, and they are not numbered. This is the standard way sugars are presented in texts. Can you tell how many carbons there are in this sugar? Count the corners and don’t forget the one that’s already indicated!
If you said “five,” you are right. Ribose is a pentose (pent = five) and happens to be the sugar present in ribonucleic acid, or RNA. Think to yourself what the sugar might be in deoxyribonucleic acid, or DNA. If you thought, deoxyribose, you’d be right.
The fourth sugar given in the figure is a deoxyribose. In organic chemistry, it’s not enough to know that corners indicate carbons. Each carbon also has a specific number, which becomes important in discussions of nucleic acids. Luckily, we get to keep our carbon counting pretty simple in basic biology. To count carbons, you start with the carbon to the right of the non-carbon corner of the molecule. The deoxyribose or ribose always looks to me like a little cupcake with a cherry on top. The “cherry” is an oxygen. To the right of that oxygen, we start counting carbons, so that corner to the right of the “cherry” is the first carbon. Now, keep counting. Here’s a little test: What is hanging down from carbon 2 of the deoxyribose?
If you said a hydrogen (H), you are right! Now, compare the deoxyribose to the ribose. Do you see the difference in what hangs off of the carbon 2 of each sugar? You’ll see that the carbon 2 of ribose has an –OH, rather than an H. The reason the deoxyribose is called that is because the O on the second carbon of the ribose has been removed, leaving a “deoxyed” ribose. This tiny distinction between the sugars used in DNA and RNA is significant enough in biology that we use it to distinguish the two nucleic acids.
In fact, these subtle differences in sugars mean big differences for many biological molecules. Below, you’ll find a couple of ways that apparently small changes in a sugar molecule can mean big changes in what it does. These little changes make the difference between a delicious sugar cookie and the crunchy exoskeleton of a dung beetle.
Sugar and Fuel
A marathon runner keeps fuel on hand in the form of “carbs,” or sugars. These fuels provide the marathoner’s straining body with the energy it needs to keep the muscles pumping. When we take in sugar like this, it often comes in the form of glucose molecules attached together in a polymer called starch. We are especially equipped to start breaking off individual glucose molecules the minute we start chewing on a starch.
Double X Extra: A monomer is a building block (mono = one) and a polymer is a chain of monomers. With a few dozen monomers or building blocks, we get millions of different polymers. That may sound nutty until you think of the infinity of values that can be built using only the numbers 0 through 9 as building blocks or the intricate programming that is done using only a binary code of zeros and ones in different combinations.
Our bodies then can rapidly take the single molecules, or monomers, into cells and crack open the chemical bonds to transform the energy for use. The bonds of a sugar are packed with chemical energy that we capture to build a different kind of energy-containing molecule that our muscles access easily. Most species rely on this process of capturing energy from sugars and transforming it for specific purposes.
Polysaccharides: Fuel and Form
Plants use the Sun’s energy to make their own glucose, and starch is actually a plant’s way of storing up that sugar. Potatoes, for example, are quite good at packing away tons of glucose molecules and are known to dieticians as a “starchy” vegetable. The glucose molecules in starch are packed fairly closely together. A string of sugar molecules bonded together through dehydration synthesis, as they are in starch, is a polymer called a polysaccharide (poly = many; saccharide = sugar). When the monomers of the polysaccharide are released, as when our bodies break them up, the reaction that releases them is called hydrolysis.
Double X Extra: The specific reaction that hooks one monomer to another in a covalent bond is called dehydration synthesis because in making the bond–synthesizing the larger molecule–a molecule of water is removed (dehydration). The reverse is hydrolysis (hydro = water; lysis = breaking), which breaks the covalent bond by the addition of a molecule of water.
Although plants make their own glucose and animals acquire it by eating the plants, animals can also package away the glucose they eat for later use. Animals, including humans, store glucose in a polysaccharide called glycogen, which is more branched than starch. In us, we build this energy reserve primarily in the liver and access it when our glucose levels drop.
Whether starch or glycogen, the glucose molecules that are stored are bonded together so that all of the molecules are oriented the same way. If you view the sixth carbon of the glucose to be a “carbon flag,” you’ll see in the figure that all of the glucose molecules in starch are oriented with their carbon flags on the upper left.
The orientation of monomers of glucose in polysaccharides can make a big difference in the use of the polymer. The glucoses in the molecule on the top are all oriented “up” and form starch. The glucoses in the molecule on the bottom alternate orientation to form cellulose, which is quite different in its function from starch.
Storing up sugars for fuel and using them as fuel isn’t the end of the uses of sugar. In fact, sugars serve as structural molecules in a huge variety of organisms, including fungi, bacteria, plants, and insects.
The primary structural role of a sugar is as a component of the cell wall, giving the organism support against gravity. In plants, the familiar old glucose molecule serves as one building block of the plant cell wall, but with a catch: The molecules are oriented in an alternating up-down fashion. The resulting structural sugar is called cellulose.
That simple difference in orientation means the difference between a polysaccharide as fuel for us and a polysaccharide as structure. Insects take it step further with the polysaccharide that makes up their exoskeleton, or outer shell. Once again, the building block is glucose, arranged as it is in cellulose, in an alternating conformation. But in insects, each glucose has a little extra added on, a chemical group called an N-acetyl group. This addition of a single functional group alters the use of cellulose and turns it into a structural molecule that gives bugs that special crunchy sound when you accidentally…ahem…step on them.
These variations on the simple theme of a basic carbon-ring-as-building-block occur again and again in biological systems. In addition to serving roles in structure and as fuel, sugars also play a role in function. The attachment of subtly different sugar molecules to a protein or a lipid is one way cells communicate chemically with one another in refined, regulated interactions. It’s as though the cells talk with each other using a specialized, sugar-based vocabulary. Typically, cells display these sugary messages to the outside world, making them available to other cells that can recognize the molecular language.
Lipids: The Fatty Trifecta
Starch makes for good, accessible fuel, something that we immediately attack chemically and break up for quick energy. But fats are energy that we are supposed to bank away for a good long time and break out in times of deprivation. Like sugars, fats serve several purposes, including as a dense source of energy and as a universal structural component of cell membranes everywhere.
Fats: the Good, the Bad, the Neutral
Turn again to a nutrition label, and you’ll see a few references to fats, also known as lipids. (Fats are slightly less confusing that sugars in that they have only two names.) The label may break down fats into categories, including trans fats, saturated fats, unsaturated fats, and cholesterol. You may have learned that trans fats are “bad” and that there is good cholesterol and bad cholesterol, but what does it all mean?
Let’s start with what we mean when we say saturated fat. The question is, saturated with what? There is a specific kind of dietary fat call the triglyceride. As its name implies, it has a structural motif in which something is repeated three times. That something is a chain of carbons and hydrogens, hanging off in triplicate from a head made of glycerol, as the figure shows. Those three carbon-hydrogen chains, or fatty acids, are the “tri” in a triglyceride. Chains like this can be many carbons long.
Double X Extra: We call a fatty acid a fatty acid because it’s got a carboxylic acid attached to a fatty tail. A triglyceride consists of three of these fatty acids attached to a molecule called glycerol. Our dietary fat primarily consists of these triglycerides.
Triglycerides come in several forms. You may recall that carbon can form several different kinds of bonds, including single bonds, as with hydrogen, and double bonds, as with itself. A chain of carbon and hydrogens can have every single available carbon bond taken by a hydrogen in single covalent bond. This scenario of hydrogen saturation yields a saturated fat. The fat is saturated to its fullest with every covalent bond taken by hydrogens single bonded to the carbons.
Saturated fats have predictable characteristics. They lie flat easily and stick to each other, meaning that at room temperature, they form a dense solid. You will realize this if you find a little bit of fat on you to pinch. Does it feel pretty solid? That’s because animal fat is saturated fat. The fat on a steak is also solid at room temperature, and in fact, it takes a pretty high heat to loosen it up enough to become liquid. Animals are not the only organisms that produce saturated fat–avocados and coconuts also are known for their saturated fat content.
The top graphic above depicts a triglyceride with the glycerol, acid, and three hydrocarbon tails. The tails of this saturated fat, with every possible hydrogen space occupied, lie comparatively flat on one another, and this kind of fat is solid at room temperature. The fat on the bottom, however, is unsaturated, with bends or kinks wherever two carbons have double bonded, booting a couple of hydrogens and making this fat unsaturated, or lacking some hydrogens. Because of the space between the bumps, this fat is probably not solid at room temperature, but liquid.
You can probably now guess what an unsaturated fat is–one that has one or more hydrogens missing. Instead of single bonding with hydrogens at every available space, two or more carbons in an unsaturated fat chain will form a double bond with carbon, leaving no space for a hydrogen. Because some carbons in the chain share two pairs of electrons, they physically draw closer to one another than they do in a single bond. This tighter bonding result in a “kink” in the fatty acid chain.
In a fat with these kinks, the three fatty acids don’t lie as densely packed with each other as they do in a saturated fat. The kinks leave spaces between them. Thus, unsaturated fats are less dense than saturated fats and often will be liquid at room temperature. A good example of a liquid unsaturated fat at room temperature is canola oil.
A few decades ago, food scientists discovered that unsaturated fats could be resaturated or hydrogenated to behave more like saturated fats and have a longer shelf life. The process of hydrogenation–adding in hydrogens–yields trans fat. This kind of processed fat is now frowned upon and is being removed from many foods because of its associations with adverse health effects. If you check a food label and it lists among the ingredients “partially hydrogenated” oils, that can mean that the food contains trans fat.
Double X Extra: A triglyceride can have up to three different fatty acids attached to it. Canola oil, for example, consists primarily of oleic acid, linoleic acid, and linolenic acid, all of which are unsaturated fatty acids with 18 carbons in their chains.
Why do we take in fat anyway? Fat is a necessary nutrient for everything from our nervous systems to our circulatory health. It also, under appropriate conditions, is an excellent way to store up densely packaged energy for the times when stores are running low. We really can’t live very well without it.
Phospholipids: An Abundant Fat
You may have heard that oil and water don’t mix, and indeed, it is something you can observe for yourself. Drop a pat of butter–pure saturated fat–into a bowl of water and watch it just sit there. Even if you try mixing it with a spoon, it will just sit there. Now, drop a spoon of salt into the water and stir it a bit. The salt seems to vanish. You’ve just illustrated the difference between a water-fearing (hydrophobic) and a water-loving (hydrophilic) substance.
Generally speaking, compounds that have an unequal sharing of electrons (like ions or anything with a covalent bond between oxygen and hydrogen or nitrogen and hydrogen) will be hydrophilic. The reason is that a charge or an unequal electron sharing gives the molecule polarity that allows it to interact with water through hydrogen bonds. A fat, however, consists largely of hydrogen and carbon in those long chains. Carbon and hydrogen have roughly equivalent electronegativities, and their electron-sharing relationship is relatively nonpolar. Fat, lacking in polarity, doesn’t interact with water. As the butter demonstrated, it just sits there.
There is one exception to that little maxim about fat and water, and that exception is the phospholipid. This lipid has a special structure that makes it just right for the job it does: forming the membranes of cells. A phospholipid consists of a polar phosphate head–P and O don’t share equally–and a couple of nonpolar hydrocarbon tails, as the figure shows. If you look at the figure, you’ll see that one of the two tails has a little kick in it, thanks to a double bond between the two carbons there.
Phospholipids form a double layer and are the major structural components of cell membranes. Their bend, or kick, in one of the hydrocarbon tails helps ensure fluidity of the cell membrane. The molecules are bipolar, with hydrophilic heads for interacting with the internal and external watery environments of the cell and hydrophobic tails that help cell membranes behave as general security guards.
The kick and the bipolar (hydrophobic and hydrophilic) nature of the phospholipid make it the perfect molecule for building a cell membrane. A cell needs a watery outside to survive. It also needs a watery inside to survive. Thus, it must face the inside and outside worlds with something that interacts well with water. But it also must protect itself against unwanted intruders, providing a barrier that keeps unwanted things out and keeps necessary molecules in.
Phospholipids achieve it all. They assemble into a double layer around a cell but orient to allow interaction with the watery external and internal environments. On the layer facing the inside of the cell, the phospholipids orient their polar, hydrophilic heads to the watery inner environment and their tails away from it. On the layer to the outside of the cell, they do the same.
As the figure shows, the result is a double layer of phospholipids with each layer facing a polar, hydrophilic head to the watery environments. The tails of each layer face one another. They form a hydrophobic, fatty moat around a cell that serves as a general gatekeeper, much in the way that your skin does for you. Charged particles cannot simply slip across this fatty moat because they can’t interact with it. And to keep the fat fluid, one tail of each phospholipid has that little kick, giving the cell membrane a fluid, liquidy flow and keeping it from being solid and unforgiving at temperatures in which cells thrive.
Steroids: Here to Pump You Up?
Our final molecule in the lipid fatty trifecta is cholesterol. As you may have heard, there are a few different kinds of cholesterol, some of which we consider to be “good” and some of which is “bad.” The good cholesterol, high-density lipoprotein, or HDL, in part helps us out because it removes the bad cholesterol, low-density lipoprotein or LDL, from our blood. The presence of LDL is associated with inflammation of the lining of the blood vessels, which can lead to a variety of health problems.
But cholesterol has some other reasons for existing. One of its roles is in the maintenance of cell membrane fluidity. Cholesterol is inserted throughout the lipid bilayer and serves as a block to the fatty tails that might otherwise stick together and become a bit too solid.
Cholesterol’s other starring role as a lipid is as the starting molecule for a class of hormones we called steroids or steroid hormones. With a few snips here and additions there, cholesterol can be changed into the steroid hormones progesterone, testosterone, or estrogen. These molecules look quite similar, but they play very different roles in organisms. Testosterone, for example, generally masculinizes vertebrates (animals with backbones), while progesterone and estrogen play a role in regulating the ovulatory cycle.
Double X Extra: A hormone is a blood-borne signaling molecule. It can be lipid based, like testosterone, or short protein, like insulin.
As you progress through learning biology, one thing will become more and more clear: Most cells function primarily as protein factories. It may surprise you to learn that proteins, which we often talk about in terms of food intake, are the fundamental molecule of many of life’s processes. Enzymes, for example, form a single broad category of proteins, but there are millions of them, each one governing a small step in the molecular pathways that are required for living.
Levels of Structure
Amino acids are the building blocks of proteins. A few amino acids strung together is called a peptide, while many many peptides linked together form a polypeptide. When many amino acids strung together interact with each other to form a properly folded molecule, we call that molecule a protein.
For a string of amino acids to ultimately fold up into an active protein, they must first be assembled in the correct order. The code for their assembly lies in the DNA, but once that code has been read and the amino acid chain built, we call that simple, unfolded chain the primary structure of the protein.
This chain can consist of hundreds of amino acids that interact all along the sequence. Some amino acids are hydrophobic and some are hydrophilic. In this context, like interacts best with like, so the hydrophobic amino acids will interact with one another, and the hydrophilic amino acids will interact together. As these contacts occur along the string of molecules, different conformations will arise in different parts of the chain. We call these different conformations along the amino acid chain the protein’s secondary structure.
Once those interactions have occurred, the protein can fold into its final, or tertiary structure and be ready to serve as an active participant in cellular processes. To achieve the tertiary structure, the amino acid chain’s secondary interactions must usually be ongoing, and the pH, temperature, and salt balance must be just right to facilitate the folding. This tertiary folding takes place through interactions of the secondary structures along the different parts of the amino acid chain.
The final product is a properly folded protein. If we could see it with the naked eye, it might look a lot like a wadded up string of pearls, but that “wadded up” look is misleading. Protein folding is a carefully regulated process that is determined at its core by the amino acids in the chain: their hydrophobicity and hydrophilicity and how they interact together.
In many instances, however, a complete protein consists of more than one amino acid chain, and the complete protein has two or more interacting strings of amino acids. A good example is hemoglobin in red blood cells. Its job is to grab oxygen and deliver it to the body’s tissues. A complete hemoglobin protein consists of four separate amino acid chains all properly folded into their tertiary structures and interacting as a single unit. In cases like this involving two or more interacting amino acid chains, we say that the final protein has a quaternary structure. Some proteins can consist of as many as a dozen interacting chains, behaving as a single protein unit.
A Plethora of Purposes
What does a protein do? Let us count the ways. Really, that’s almost impossible because proteins do just about everything. Some of them tag things. Some of them destroy things. Some of them protect. Some mark cells as “self.” Some serve as structural materials, while others are highways or motors. They aid in communication, they operate as signaling molecules, they transfer molecules and cut them up, they interact with each other in complex, interrelated pathways to build things up and break things down. They regulate genes and package DNA, and they regulate and package each other.
As described above, proteins are the final folded arrangement of a string of amino acids. One way we obtain these building blocks for the millions of proteins our bodies make is through our diet. You may hear about foods that are high in protein or people eating high-protein diets to build muscle. When we take in those proteins, we can break them apart and use the amino acids that make them up to build proteins of our own.
How does a cell know which proteins to make? It has a code for building them, one that is especially guarded in a cellular vault in our cells called the nucleus. This code is deoxyribonucleic acid, or DNA. The cell makes a copy of this code and send it out to specialized structures that read it and build proteins based on what they read. As with any code, a typo–a mutation–can result in a message that doesn’t make as much sense. When the code gets changed, sometimes, the protein that the cell builds using that code will be changed, too.
Biohazard!The names associated with nucleic acids can be confusing because they all start with nucle-. It may seem obvious or easy now, but a brain freeze on a test could mix you up. You need to fix in your mind that the shorter term (10 letters, four syllables), nucleotide, refers to the smaller molecule, the three-part building block. The longer term (12 characters, including the space, and five syllables), nucleic acid, which is inherent in the names DNA and RNA, designates the big, long molecule.
DNA vs. RNA: A Matter of Structure
DNA and its nucleic acid cousin, ribonucleic acid, or RNA, are both made of the same kinds of building blocks. These building blocks are called nucleotides. Each nucleotide consists of three parts: a sugar (ribose for RNA and deoxyribose for DNA), a phosphate, and a nitrogenous base. In DNA, every nucleotide has identical sugars and phosphates, and in RNA, the sugar and phosphate are also the same for every nucleotide.
So what’s different? The nitrogenous bases. DNA has a set of four to use as its coding alphabet. These are the purines, adenine and guanine, and the pyrimidines, thymine and cytosine. The nucleotides are abbreviated by their initial letters as A, G, T, and C. From variations in the arrangement and number of these four molecules, all of the diversity of life arises. Just four different types of the nucleotide building blocks, and we have you, bacteria, wombats, and blue whales.
RNA is also basic at its core, consisting of only four different nucleotides. In fact, it uses three of the same nitrogenous bases as DNA–A, G, and C–but it substitutes a base called uracil (U) where DNA uses thymine. Uracil is a pyrimidine.
DNA vs. RNA: Function Wars
An interesting thing about the nitrogenous bases of the nucleotides is that they pair with each other, using hydrogen bonds, in a predictable way. An adenine will almost always bond with a thymine in DNA or a uracil in RNA, and cytosine and guanine will almost always bond with each other. This pairing capacity allows the cell to use a sequence of DNA and build either a new DNA sequence, using the old one as a template, or build an RNA sequence to make a copy of the DNA.
These two different uses of A-T/U and C-G base pairing serve two different purposes. DNA is copied into DNA usually when a cell is preparing to divide and needs two complete sets of DNA for the new cells. DNA is copied into RNA when the cell needs to send the code out of the vault so proteins can be built. The DNA stays safely where it belongs.
RNA is really a nucleic acid jack-of-all-trades. It not only serves as the copy of the DNA but also is the main component of the two types of cellular workers that read that copy and build proteins from it. At one point in this process, the three types of RNA come together in protein assembly to make sure the job is done right.
Over the last few months, the concept of birth control has been under great scrutiny in the American eye. Many politicians have been discussing it’s “moral” implications, and whether institutions or organizations should have the right to deny insurance coverage for hormonal contraception if it does not fall within the confines of their belief systems. And while American women have narrowly escaped legislation that would impede their reproductive health and freedom, politicians, mostly men, feel it necessary to make misinformed or even completely false statements about birth control.
For some strange reason, there is this erroneous idea that birth control is not a matter of health, but rather a means by which a woman can engage in careless and frequent sexual activity, with a man, and without the consequences of pregnancy. It’s clear that the picture these politicians are trying to paint is that of debauchery and immorality, which, of course, is a departure from the puritanical integrity they embody. But, rather than focus on this utter nonsense, I would prefer to highlight the significant impact birth control will have on the future of our civilization and our planet.
The human population has grown steadily since the beginning of our species. However, the rate of growth began to skyrocket after the industrial revolution, and our population has actually doubled over the last 50 years, reaching 7 the billion mark in March of this year. This is an astounding statistic since it took until 1804 – around 50,000 years – to reach our first billion.
World Population: 1800 – 2100 (Wikimedia Commons)
What makes these numbers really scary is the concept of carrying capacity, which is an ecological term used to describe the maximum number of individual members of a species that a certain habitat can support. In this case, the species is human and that certain habitat is planet earth.
Here’s the thing: the availability of our resources will not match the rate of population growth. Given our current technologies, there is only so much food we can grow, only so much water we can drink, only so much space we can inhabit, only so much waste we can safely rid, only so much energy we can harness. There will be a point that the human population will hit its carrying capacity on earth, and when it does, the chances of widespread famine will be great, and the delineation between the developing world and the developed world will be no longer.
Given this very serious issue, Britain’s Royal Society has recently convened to discuss the future of the human population and on April 26th, 2012, and published their findings in the People and the Planet Report [PDF]. For me, key findingnumber three struck a cord:
Reproductive health and voluntary family planning programmes urgently require political leadership and financial commitment, both nationally and internationally. This is needed to continue the downward trajectory of fertility rates, especially in countries where the unmet need for contraception is high. (emphasis theirs)
Political leadership and financial commitment – Did you see that, American politicians?? For those of you who are unnecessarily waging war on women’s reproductive rights, its time to get your giant heads out of your collective asses and realize the implications of legislation that would go against ensuring both the continued success of our species and the health of our planet. It is time to stop spending money on these regressive and oppressive campaigns guised under the false pretense of “religious freedom” and start making a financial commitment to the women (and by association, men) who live in our nation.
To drive this point even further, here is another excerpt from the People and the Planet Report (my favorite bit, found in Box 2.5 on page 33):
Women bear the main physical burden of reproduction: pregnancy, breastfeeding and childcare. They also bear the main responsibility for contraception as most methods are designed for their use. Men, it may be argued, reap the benefits of children without incurring an equal share of the cost. It follows that women may be more favourable to the idea of small families and family planning than their partners but unable to express their inclinations in male-dominated systems. Such views received international endorsement in the Program of Action resulting from the UN conference on population in 1994. Paragraph 4.1 states that “improving the status of women is essential for the long-term success of population programs”.
We currently live in a nation where 99% of women who are of reproductive age have used some form of birth control at least once. And when it comes to hormonal contraception, over 80% of sexually active women aged 15-44 have relied on “the pill” as a means to prevent unwanted pregnancies. This has contributed to an average of two births per American woman, which is considered to be the replacement rate for a population. Compare this number to countries where birth control and reproductive education is scarce – countries like Niger (7.52 births per woman) or Afghanistan (5.64 births per woman) – and one can see the impact of family planning through contraception. Furthermore, it has been well documented that women in developed worlds who are provided with the means to control their fertility are more empowered and their families are healthier.
While our situation in the US is significantly better compared to underdeveloped nations where rape and the cultural devaluing of women is commonplace, we still have a responsibility to uphold – a responsibility that would undoubtedly increase the quality of life for women (and men), as well as contribute to the overall health of the human population. Why would we want to go backwards and remove the ability of a woman to decide when, if ever, she would like to reproduce?
Having access to birth control empowers women and allows them to make greater contributions to society. And because contraception is primarily the responsibility of a woman, our society needs to ensure that birth control, reproductive education, and family planning resources are readily available to EVERYONE.
The United Nations predicts that the ten-billionth person will be born around 2050. Will we continue to fight this ridiculous fight against women’s rights or will we redirect our collective energy to developing technologies that will help our species and planet better cope with the increasing demands associated with a steadily rising population? Let’s stop allowing stupidity to prevail and let’s start doing the right thing: making sure that birth control is readily available to any woman who wishes to use it. Because, now more than ever, it is clear that birth control will save the world.
Note: In my readings for this article, I came across a wonderful resource for anyone interested in learning more about human fertility and population growth. Through the wonders of the internet, Academic Earth is offering a free (!) online course called Global Population Growth, given by Yale University professor Robert Wyman.
These views are the opinion of the author and do not necessarily either reflect or disagree with those of the DXS editorial team.
A scanning electron micrograph of a blood clot. Image credit: Steve Gschmeissner/Science Photo Library (http://www.sciencephoto.com/media/203271/enlarge#)
On Monday January 1st, I overheard my dad telling my mom how his left arm was numb and that he had no strength in his left hand. I immediately ran into the medicine cabinet, grabbed two aspirin, practically shoved them down my dad’s throat, and told him to get his coat. He was going to the ER.
As it turns out, my dad was having a stroke, which is basically the cessation of blood flow to an area in the brain. Luckily, my dad only suffered a very mild stroke, and after several days of monitoring and a battery of tests, he was released from the hospital.
While we are all relieved that he dodged what could have been a fatal bullet, I came to realize that there was only a superficial understanding of what was actually happening. So, to help demystify the process for my dad (and anyone else in this situation), I’ve decided to write a mini-guide on strokes. Below you will find some handy information about strokes, including what they are, as well as a glossary of relevant terms.
Why we need blood flow in the brain
Before I get into what happens to the brain when a stroke occurs, it is important to first understand why unrestricted blood flow in blood vessels in the brain is important. The brain is a type of tissue, and like all tissues in our body, it needs a constant access to nutrients and oxygen. Furthermore, tissues produce waste, and this waste needs to be removed.
The human cardiovascular system. Image Credit: Wikipedia.
Evolution’s solution to this problem is the development of a vast network of blood vessels existing within our tissues. For instance, take a good look at your very own eyeballs. Especially when we are tired, we can see tiny blood vessels called capillaries, which help to deliver key nutrients and oxygen, keeping our organs of sight healthy and happy. Now consider that this type of blood vessel network exists in all tissues in our bodies (because it does). Depending on the needs of the tissue, these vessels vary in size and number. Sometimes the blood vessels are large, like the aorta, and sometimes they are super tiny, like the capillaries in our eyes. However, all serve the same function: to make sure that cells can breath, eat, and get rid of waste.
When blood is prevented from traveling to a specific area within a tissue, the cells in that area will not get enough fuel and oxygen and will begin to die. For instance, the restriction of blood flow to the heart leads to the death of heart tissue, causing a heart attack. Similarly, the interruption of normal blood flow within the brain causes the affected cells in the brain to essentially starve, suffocate, and die, resulting in a stroke. The medical term for a lack of oxygen delivery to tissues due to a restriction in blood flow is ischemia. In general, the heart, brain, and the kidneys are the most sensitive to ischemic events, which, when occurring in these organs, can be fatal.
So, what exactly is a stroke?
Some strokes can be categorized as being ischemic. As mentioned above, an ischemic stroke occurs when blood flow (and the associated oxygen supply) is restricted in an area within the brain, leading to tissue death. A major cause of ischemic strokes is a progressive disease called atherosclerosis, which can be translated to mean “the hardening of the arteries.”
Severe atherosclerosis of the aorta. Image Credit: Wikipedia.
Affecting the entire cardiovascular system, atherosclerosis is the result of cholesterol build-up inside of our blood vessels, causing their openings to become narrower. These cholesterol plaques can eventually burst, leading to the formation of a blood clot. Ischemic strokes occur as a result of a blood clot, medically known as a thrombus, that blocks the flow of blood to the brain, a phenomenon often related to complications from atherosclerosis. A ruptured cholesterol plaque and resulting blood clot can occur in the brain, or it can occur elsewhere in the body, such as in the carotid arteries, and then travel to the brain. Either way, the blood clot will block blood flow and oxygen delivery to sensitive brain tissue and cause a stroke.
Strokes that result from the bursting of a blood vessel in the brain can be categorized as being hemorrhagic. In this situation, there may be a pre-existing condition rendering the blood vessels in the brain defective, causing them to become weak and more susceptible to bursting. More often than not, a hemorrhagic stroke is the result of high blood pressure, which puts an awful lot of stress on the blood vessels. Hemorrhagic strokes are less common than ischemic strokes, but still just as serious.
How do you know if you’ve had a stroke?
The symptoms of a stroke can vary depending on which part of the brain is affected and can develop quite suddenly. It is common to experience a moderate to severe headache, especially if you are hemorrhaging (bleeding) in the brain. Other symptoms can include dizziness, a change in senses (hearing, seeing, tasting), muscle tingling and/or weakness, trouble communicating, and/or memory loss. If you are experiencing any of these warning signs, it is important to get to the hospital right away. This is especially important if the stroke is being caused by a blood clot since clot-busting medicationsare only effective within the first few hours hours of clot formation.
Once in the hospital, the caregiver will likely give anyone suspected of having a stroke a CT scan. From this test, doctors will be able to determine if you had a stroke, what type of stroke you had (ischemic versus hemorrhagic), or if there is some other issue. However, as was the case with my dad, a CT scan may not show evidence for a stroke. This issue can arise as a result of timing (test performed before brain injury set in) or size of affected area (too small to see). When not in an emergency situation, doctors may also or instead choose to prescribe an MRItest to look for evidence of a stroke.
If a stroke has been confirmed, the next steps will be to try and figure out the underlying cause. For ischemic strokes, it is important to find out if there is a blood clot and where it originated. Because my dad had an ischemic stroke, he had to undergo a series of tests that searched for a blood clot in his carotid arteries though ultrasound, as well as in the heart, using both an electrocardiogram(EKG) and an echocardiogram(ultrasound of the heart). The patient might also be asked to wear a Holter Monitor, which is a device worn for at least 24 hours and can detect potential heart abnormalities that may not be obvious from short-term observations, like those obtained via an EKG. If a stroke is due to a hemorrhagic event, an angiogramwould be performed to try an pinpoint the compromised blood vessel.
A stroke you did have. Now what?
Once a stroke has been confirmed and categorized, the patient will most likely be transferred to the stroke unit of the hospital for both treatment and further observation. If a clot has been detected, a patient will receive clot-busting medications (assuming this detection occurs within several hours of clot formation). Alternatively, a clot can be mechanically removed with surgery (animation of clot removal, also known as a thrombectomy). Patients might also be given blood-thinning medications to either ensure that clots do not increase in size or to prevent new clots from forming. As for secondary prevention, meaning preventing another stroke from happening, patients might be given blood pressure and cholesterol lowering medications.
If a disability arises due to stroke, a patient might need to undergo rehabilitation. The type and duration of stroke rehabilitation is dependent on the area of brain that was affected, as well as the severity of the injury.
Major risk factors and predictors of stroke
There are many situations that could predispose one to having a stroke, and many of these conditions are treatable. The absolute greatest predictor of a stroke is blood pressure. High blood pressure, also known as hypertension, will significantly raise your risk of having a stroke. Other modifiable stroke risk factors include blood cholesterol levels, smoking, type 2 diabetes, diet, alcohol/drug use, and a sedentary life style. However, there are also risk factors that you cannot change including family history of stroke, age, race, and gender. But that shouldn’t stop one from practicing a healthy lifestyle!
In conclusion, strokes are no joke. I am glad that my dad is still here (yes, dad, if you are reading this, we are in fact friends) and that he escaped with relatively no real consequences. Let’s just not do this again, ok?
Anti-coagulants:These are medications that help to reduce the incidence of blood clotting. The repertoire includes aspirin, Plavix, Warfarin, and Coumadin. Also called blood thinners.
Atherosclerosis:Literally translated as “hardening of the arteries,” this condition is hallmarked by the build-up of cholesterol inside of blood vessels. Atherosclerosis can lead to many complications including heart disease and stroke.
Cardiovascular System: The network of blood vessels and heart that works to distribute blood throughout the body.
Carotid Arteries: Arteries that carry blood away from the heart toward the head, neck, and brain.
CT Scan: Cross sectional pictures of the brain using X-rays.
Echocardiogram:An ultrasound of the heart. In stroke vicitms, electrocardiography is used to detect the presence of a blood clot in the heart.
Electrocardiogram (EKG or ECG): The measurement of the electrical activity of the heart. It is performed by attaching electrodes to a patient at numerous locations on the body, which function to measure electrical output of the heart.
Embolic Stroke: A type of ischemic stroke, an embolic stroke occurs when a blood clot forms (usually in the heart) and then travels to the brain, blocking blood flow and oxygen delivery to brain tissue.
Hemorrhagic Stroke: A type of stroke that results form the bursting of a blood vessel in the brain.
Hypertension:High blood pressure, defined as having 140/90 mmHg or above.